7sem sq3

49
DR. MANALI HAZARIKA SINGH

Transcript of 7sem sq3

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DR. MANALI HAZARIKA SINGH

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Incomitant squints

Variation in the amount of deviation in different directions of gaze.

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Differences Incomitant squint Comitant squint

1. Age of onset Usually late Early childhood

2. Type of onset Sudden Gradual

3. Magnitude of squint

Varies with eye position

Same in all positions

4. Diplopia Present Absent

5. Headposture Abnormal Normal

6. Sensory adaptations *

Rare Frequent

7. Past pointing/ false projection

Present Absent

8. EOM Restricted Full

9.Secondary deviation

More than primary Equal to primary

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Incomitant strabismus

Paralytic - Neurogenic, Myogenic, NMJ

Restrictive – Duane’s , Brown’s syndrome, Dysthyroid ophthalmopathy, Blow out fracture with incarceration of EOM.

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Paralytic strabismus etiology I. Neurogenic lesions 1. Congenital hypoplasia or absence of nucleus:

third and sixth cranial nerve palsies. 2. Inflammatory lesions: encephalitis,meningitis,

neurosyphilis,peripheral neuritis (viral),infectious lesions of cavernous sinus and orbit.

3. Neoplastic lesions. 4. Vascular lesions:HTN, DM and atherosclerosis. haemorrhage, thrombosis, embolism, aneurysms or vascular occlusions.

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Paralytic strabismus etiology 5. Traumatic lesions: head injury 6. Toxic lesions:carbon monoxide

poisoning, effects of diphtheria toxins (rarely),alcoholic and lead neuropathy.

7. Demyelinating lesions:multiple sclerosis II. Myogenic lesions 1. Congenital lesions. These include

absence, hypoplasia, malinsertion, weakness and

musculofacial anomalies. 2. Traumatic lesions.

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Paralytic strabismus etiology

3. Inflammatory lesions: Myositis (viral) , influenza, measles.

4. Myopathies:These include thyroid myopathy,carcinomatous myopathy,Progressive external ophthalmoplegia

III. Neuromuscular junction lesion It includes myasthenia gravis.

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Paralytic strabismus

SYMPTOMS:

1.LIMITATION OF OCULAR MOVEMENTS

2.SUDDEN ONSET OCULAR DEVIATION3.DIPLOPIA4.CONFUSION5.NAUSEA , VERTIGO

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Diplopia

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DIPLOPIA-A)Uncrossed diplopia with an esotropia.B)Crossed diplopia with an exotropia.

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Paralytic strabismus

SIGNS: Limitation of movement in the field

of action of the muscle Difference in primary and secondary

deviations Compensatory HP False projection

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FALSE PROJECTION

OBJECT IS PROJECTED TOO FAR IN THE DIRECTION OF ACTION OF THE PARALYSED MUSCLE.

DUE TO INCREASE OF SECONDARY DEVIATION , THE OBJECT IS PROJECTED ACCORDING TO THE NERVOUS ENERGY EXERTED

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Stages- SPREAD OF COMITANCE

Paresis of the particular muscle (LSO) Overaction of antagonist of same eye (LIO) Overaction of contralateral yoke

muscle(RIR) Secondary inhibitional palsy of antagonist of

the yoke muscle (RSR)

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Pathological sequelae of the right lateral rectus muscle paralysis.

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Clinical types of ocular palsies

1. Isolated muscle paralysis LR and superior oblique are the

most common muscles to be paralysed singly, as they have separate nerve supply.

Isolated paralysis of the remaining four muscles is less common, except in congenital lesions.

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Clinical types of ocular palsies

2. 3rd nerve paralysis

Ptosis Eyeball is down, out and

slightly intorted Ocular movements are

restricted in all the directions except outward.

Pupil is fixed and dilated Accommodation is lost Crossed diplopia is elicited

on raising the eyelid.

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Clinical types of ocular palsies 3. Double elevator

palsy. congenital caused by third

nerve nuclear lesion. characterised by

paresis of the superior rectus and the inferior oblique muscle of the involved eye.

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Clinical types of ocular palsies

4. Total ophthalmoplegia

extraocular muscles including LPS and intraocular muscles,

viz., sphincter pupillae, and ciliary muscle

are paralysed third, fourth and sixth

cranial nerves. orbital apex syndrome and cavernous sinus thrmb

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Clinical types of ocular palsies 5. External ophthalmoplegia. In

this condition, all extraocular muscles are paralysed,

sparing the intraocular muscles. It results from lesions at the level of

motor nuclei sparing the Edinger-Westphal

nucleus

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Investigations

Diplopia charting Hess charting Forced duction test Force generation test

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DIPLOPIA CHARTING

AREAS OF SINGLE VN AND DIPLOPIA DIST. BETWN THE TWO IMAGES IN

AREAS OF DIPLOPIA WHETHER THE IMAGES ARE AT THE

SAME LEVEL OR NOT WHETHER THE DIPLOPIA IS

HOMONYMOUS OR CROSSED

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Diplopia chart of a patient with right lateral rectus palsy.

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HESS SCREEN

DIFF. PARETIC FROM RESTRICTIVE RECENT ONSET PARESIS FROM LONG STANDING

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Hess chart

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Forced duction test

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Investigations to find out the cause of paralysis orbital ultrasonography, orbital and skull computerised

tomography scanning and neurological investigations.

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TREATMENT TREAT THE CAUSE WAIT N WATCH – 6MTHS – B

COMPLEX , SYSTEMIC STEROIDS TREAT DIPLOPIA- OCCLUDER ON THE

AFFECTED EYE WITH INTERMITTENT USE OF BOTH EYES TO AVOID SUPPRESSION AMBLYOPIA

SURGERY-STRENGTHENING OF THE PARALYSED MUSCLE - RESECTION; WEAKENING OF THE OVERACTING MUSCLE - RECESSION.

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Restrictive strabismus

Duane’s retraction syndrome Superior oblique sheath syndrome

(Brown syndrome) Blow-out fractures – incarceration of

muscle Strabismus fixus, Dysthyroid ophthalmopathy

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Duane’s retraction syndrome (DRS)

On attempted adduction there is retraction of globe : co-contraction of both MR and LR (narrowing of palpebral fissure)

On attempted abduction, the palpebral fissure opens

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DUANE’S

• FAILURE OF INNERVATION OF LR BY 6TH N 3rd N.

• Type I LIMITED ABDUCTION, NORMAL ADDUCTION, PRIMARY POSITION- N

• Type II LIMITED ADDUCTION , NORMAL ABDUCTION

• Type III LIMITED ADDUC AND ABDUC

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Brown syndrome

Superior oblique sheath syndrome A tight superior oblique sheath:

congenital or acquired Restriction of elevation in

adduction Positive forced duction test

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Strabismus fixus

Bilateral fixation in convergent position due to fibrous tightening of the medial recti

The cornea was completely hidden in the right eye and only 2 mm of the superotemporal cornea was detectable in the left eye

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BLOW OUT FRACTURE

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SYNKINESES

Involuntary movement of muscles or limbs accompanying a voluntary movement.

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Nystagmus

DEFN: Regular , rhythmic, to and fro involuntary oscillatory movements of the eyes.

ETIO: Disturbance of factors responsible for maintaining normal ocular posture-sensory visual pathway, vestibular apparatus,semicircular canals,midbrain, cerebellum

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Features of nystagmus

Pendular/Jerk Rotatory/Horizontal/ Vertical Rapid/slow Latent/Manifest

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TYPES OF NYSTAGMUS

1.PHYSIOLOGICAL NYSTAGMUS

A) OPTOKINETIC NYSTAGMUS B) END POINT NYSTAGMUS C) VESTIBULAR NYSTAGMUS

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2. Pathological Sensory deprivation

Horizontal and pendular Central vision impairment in <2yr age *

Motor imbalance /neurologic diseases Congenital nystagmus / manifest nystagmus Latent nystagmus (congenital esotropia) Vestibular nystagmus Upbeat nystagmus Downbeat nystagmus See saw nystagmus of Maddox Convergence- retraction nystagmus Periodic alternating nystagmus Gaze evoked nystagmus Miner’s nystagmus

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THANK YOU

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Alphabet patterns : A-V

V pattern: difference in deviation in the upgaze and downgaze of >15 prism dioptres

A pattern: difference in deviation in the upgaze and downgaze of >10 PD

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CAUSES

IOOA SO UNDERACTION SR UNDERACTION BROWN SYNDROME CRANIOFACIAL ANOMALIES

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A PATTERN

CAUSES SOOA IO UNDERACTION IR UNDERACTION

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