This document discusses motor adaptation in paresis and non-paresis strabismus. It begins by defining strabismus and describing the different types. It then discusses the consequences of strabismus and the different ways motor adaptation occurs, including through changes in muscle tone, compensatory head posture, and blind spot mechanisms. It describes how motor adaptation occurs differently in incomitant versus comitant strabismus. The document goes on to discuss various cranial nerve palsies and how they result in specific eye positions and compensatory head postures. It also covers special restrictive disorders like Duane's retraction syndrome.
Accommodation/ Accommodation of Eye, Measurement of Accommodation of Eye (hea...Bikash Sapkota
CLICK HERE TO DOWNLOAD FULL PPT ❤❤ https://healthkura.com/measurement-of-accommodation-of-eye/ ❤❤
Dear viewers Check Out my other piece of works at ❤❤❤ https://healthkura.com ❤❤❤
Measurement of Accommodation of eye:
Amplitude, Facility,
Relative Accommodation, Fatigue, Lag,
Dynamic Retinoscopy
Presentation Layout:
-Introduction to accommodation of eye
-Mechanism
-Components
-Measurement of accommodation of eye
- Amplitude
- Facility
- Relative accommodation
- Lag
-Dynamic Retinoscopy
Accommodation
-dioptric adjustment of the crystalline lens of the eye
- to obtain clear vision for a given target of regard
-process by which the refractive power of eye is altered
- to ensure a clear retinal image
For further reading
-Clinical Procedures in Optometry by J.D. Bartlett, J.B. Eskridge, J.F. Amos
-Primary Care Optometry by Theodere Grosvenor
-Borish’s Clinical Refraction by W.J. Benjamin
-Clinical Procedures for Ocular examination by Carlson et al
-American Academy of Ophthalmology
-Optometric Clinical Practice Guideline by American Optometric Association
-Internet
Follow me to get in touch with optometric and ophthalmic updates
Accommodation/ Accommodation of Eye, Measurement of Accommodation of Eye (hea...Bikash Sapkota
CLICK HERE TO DOWNLOAD FULL PPT ❤❤ https://healthkura.com/measurement-of-accommodation-of-eye/ ❤❤
Dear viewers Check Out my other piece of works at ❤❤❤ https://healthkura.com ❤❤❤
Measurement of Accommodation of eye:
Amplitude, Facility,
Relative Accommodation, Fatigue, Lag,
Dynamic Retinoscopy
Presentation Layout:
-Introduction to accommodation of eye
-Mechanism
-Components
-Measurement of accommodation of eye
- Amplitude
- Facility
- Relative accommodation
- Lag
-Dynamic Retinoscopy
Accommodation
-dioptric adjustment of the crystalline lens of the eye
- to obtain clear vision for a given target of regard
-process by which the refractive power of eye is altered
- to ensure a clear retinal image
For further reading
-Clinical Procedures in Optometry by J.D. Bartlett, J.B. Eskridge, J.F. Amos
-Primary Care Optometry by Theodere Grosvenor
-Borish’s Clinical Refraction by W.J. Benjamin
-Clinical Procedures for Ocular examination by Carlson et al
-American Academy of Ophthalmology
-Optometric Clinical Practice Guideline by American Optometric Association
-Internet
Follow me to get in touch with optometric and ophthalmic updates
It describes about the procedure of Hess charting. it serves as a great tool to understand the concepts involved. Suitable for optometry course. This is not a routine procedure but an important procedure which is used in diagnosis.
Detailed instumentaion and use of manual Lensometer and just a outline of automated lensometer.
I have used the picture of manual lensometer with out the parts describtion because i have explained orally by showing the picture..
Hope u all like it and may help you in learning better. :)
It describes about the procedure of Hess charting. it serves as a great tool to understand the concepts involved. Suitable for optometry course. This is not a routine procedure but an important procedure which is used in diagnosis.
Detailed instumentaion and use of manual Lensometer and just a outline of automated lensometer.
I have used the picture of manual lensometer with out the parts describtion because i have explained orally by showing the picture..
Hope u all like it and may help you in learning better. :)
In this talk, we'll go from finding a need for navbar support in ember-bootstrap to writing it. Along the way, we'll address technical challenges like multi-level action passing and making component state visible through component closures. By the end, we'll see how relentlessly pursuing usage ergonomics leads to a clean solution with contextual components and the testing questions that carries with it.
E360 es un estudio de fotografía enfocado en Fotografía Hotelera. A través de nuestras fotografías, buscamos resaltar los mejores detalles de cada uno de los espacios, dándole una gran prioridad a las experiencias que se pueden vivir en cada uno de ellos.
To Know about Extra Ocular muscles
To Know about Ocular Motility & Laws of OM
To Know various Cardinal Gaze of OM
An Idea OM Disorder (Children+ Adult)
Treating protocol OM Disorder
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Motor adaptation in paretic and nonparetic strabismus
1. K O P I L A K A F L E
B . O P T O M E T R Y
T H I R D Y E A R
MOTOR ADAPTATION IN
PARETIC AND NONPARETIC
STRABISMUS
Moderator :
Mr. Gaurishankhar Shrestha
3. STRABISMUS
Aka SQUINT is deviation of eye
Misalignment of the visual axes of the two eyes
4. TYPES OF STRABISMUS
Can be COMITANT or INCOMITANT
INCOMITANT COMITANT
Results when there is limitation of
ocular movement
Result of abnormality in
establishment of normal BSV
Can be paralytic or non paralytic Always non paralytic
limitation of ocular movement normal extraocular motility
particular abnormal head posture
develops ,I.E motor adatation occurs
no head posture ,instead sensory
adaptation occurs
Muscle sequelae present in old cases Absence of muscle sequelae
5. EXAMPLES
INCOMITANT STRABISMUS COMITANT STRABISMUS
A . NEUROGENIC A . PRIMARY STRABISMUS
due to palsy of third ,fourth and
sixth cranial nerve
B . MYOGENIC B . SECONDARY STRABISMUS
due to problem affecting muscle
itself
C . MECHANICAL C .CONSECUTIVE STRABISMUS
due to interference with muscle
contraction and relaxation
10. WAYS OF MOTOR ADAPTATION
Control of ocular deviation by an alteration of tone of
extraocular muscles
Compensatory head posture
Blind spot syndrome
Blind spot mechanism
11. Control of ocular deviation by an alteration of
tone of EOM
Can control only small degree of ocular deviation
active contraction or an active relaxation
compelling fusion reflexes
disappearance of squint(manifest
deviation converted to latent one)
12. BLIND SPOT SYNDROME
In esotropia of 12 – 18 ˚ with good visual acuity in
both eye
Normal retinal correspondence and normal fusional
vergence present
Eye further moved to esotropic side projecting
image seen by deviating eye onto blind spot
13.
14. BLIND SPOT MECHANISM
Coincidental type of esotropia
Image of fixated object falls on the blind spot
15. BLIND SPOT SYNDROME BLIND SPOT MECHANISM
Good visual acuity in both eyes Amblyopia of the non dominant eye
Normal retinal correspondence Abnormal retinal correspondence
No suppression other than fovea of the
deviated eye
ARC and suppression may coexist
16. Compensatory head posture
Used by visually mature patients(does not
necessarily develops in every patients)
Occurs in paralytic strabismus and alphabet
pattern strabismus
Has 3 components
18. WHAT ACTUALLY IS PARALYSIS?
Malfunctioning or dysfunctioning of nerves
Paralysis = no movement is possible
Paretic = some movement is possible
Palsy = includes both paresis and paralysis
(generally used )
20. TO KNOW THIS FIRST WE MUST
KNOW ACTIONS OF
EXTRAOCULAR MUSCLES
WHAT HAPPENS WHEN THESE
NERVES GET PARALYSED?
21. ACTIONS OF EOM
LATERAL RECTUS
AND MEDIAL
RECTUS HAVE
ONLY PRIMARY
ACTIONS
MEDIAL RECTUS adducts
the eye
LATERAL RECTUS abducts
the eye
22. NOTES
Vertical rectus i.e superior and inferior rectus have
their primary function as elevator and depressor
while secondary action as intorsion and extorsion
For oblique muscle opposite is true
SIN : all superiors are intorters
RAD : all vertical rectus are adducters
23. LET’S TRY THEN….
SUPERIOR RECTUS
A. ELEVATOR
B. INTORTER
C. ADDUCTOR
INFERIOR RECTUS
A. DEPRESSOR
B. EXTORTER
C. ADDUCTOR
SUPERIOR OBLIQUE
A. INTORSION
B. DEPRESSOR
C. ABDUCTION
INFERIOR OBLIQUE
A. EXTORSION
B. ELEVATOR
C. ABDUCTION
24.
25. IN CASE OF PALSY,
Actions of muscles interrupted
SO, eye takes its position opposite to its action
For example,in LR palsy,eye is in adducted position
in MR palsy,eye is in abducted position
26. QUESTIONS
WHAT IS EYE POSITION
IN SUPERIOR RECTUS
PALSY?
DEPRESSED
EXTORTED
ABDUCTED
WHAT IS EYE POSITION IN
INFERIOR OBLIQUE PALSY?
INTORTED
DEPRESSED
ADDUCTED
27. Less to be worried about…
In case of palsy, there is usually some direction of
binocular gaze in which the visual axes are
approximately parallel in which BSV can be
obtained
COMPENSATORY HEAD POSTURE
28. Normal effect of tilting the head
LE is extorted ,so tilting
to the right overcomes
this disability,visual axes
of both eye parallel
29. In primary
position without
head posture,LE
hypotropic
In
dextroversion
,parallelism of
visual axes
Updrift of
right eye in
laevoversion
Congenital
paresis of left
superior rectus,
motor adapted
condition
30. REASONS FOR AHP
TO ACHIEVE BSV :
Head turned into the field of action
of paralysed muscle
Eyes directed by DOLL’S HEAD
PHENOMENON
Patient’s limited field of single
vision coincides with his egocentric
position
Occurs when patient fixates with
normal eye
TO ACHIEVE WIDE
SEPARATION OF DIPLOPIC
IMAGES
In patients with no useful field of
vision
Turn the head opposite to the
field of paretic muscle
Deviation of the eye maximum
Occurs when patient fixates with
affected eye
31. DOLL’S HEAD PHENOMENON
Aka tonic movements
Influenced by labyrinthine reflex from otoliths
When head is rotated to the right,the eye will rotate
to the left and vice-versa
If the head is tipped backward, the eyes will rotate
downward and vice-versa
32.
33. ALSO KEEP IN MIND
When head is
tilted to the
right shoulder,
right eye intorts
while left eye
extorts…..and
vice - versa
34.
35. IN HORIZONTAL RECTUS PALSY
Only one component of abnormal head posture
i.e face/head turn
Face turn towards the action of paretic muscle
Head turn to right :
- to maintain an ocular posture
of laevoversion
-compensate for defective
abduction of RE or defective
adduction of LE
36. To conclude,
Esotropic eye is made more esotropic
Exotropic eye is made more exotropic,
BUT,
BE CAREFUL
It’s not true in case of cyclovertical muscle
37. Head turn in case of cyclovertical muscle
Head is turned such that
eyes are brought away
from field in which
muscle has its greatest
vertical effect.
Right superior rectus palsy
38. e.g. for vertical rectus , having maximum effect on
abduction,face is turned so that involved eye is
adducted
i.e face is turned towards the affected eye
WHILE , for oblique muscles, having maximum effect
on adduction , face is turned such that the involved
eye is abducted
i.e face is turned away from affected eye
39. IN PALSY OF CYCLOVERTICAL MUSCLE
Has all 3 components of abnormal head posture i.e
chin elevation or depression , face turn and head tilt
40. CHIN ELEVATION
As chin is elevated , eye
moves down
Occurs to maintain eye
posture of depression to
compensate for defective
elevation of eye(s)
To conclude , hypotropic
eye is eye is made more
hypotropic
41. CHIN DEPRESSION
In chin depression , eye moves up
Adopted to maintain ocular posture of elevation to
compensate for defective depression of eye(s)
To conclude hypertropic eye is made more
hypertropic
42. HEAD TILT
In paresis of oblique muscle,
head tilt occurs to compensate the torsion caused
by the direct antagonist of paralysed muscle
E.g.in RSO palsy,head tilt occurs to the left to
compensate for the extorsion caused by RIO muscle
To conclude, extorted eye is made more extorted and
intorted eye made more intorted BUT,its not true for
vertical rectus muscle
43. In paresis of vertical rectus muscle ,
head tilt occurs to compensate the
torsion caused by contralateral anatagonist of the
paralysed muscle
E.g in paresis of RSR, head tilt occurs to right to
compensate for the extorsion of the left eye caused
by overacting LIO muscle
To conclude,head is tilted to the side of hypotropic eye
44. Muscle
paralysed
Chin Face turn Head tilt
RSR elevation right right
RIR depression right left
RSO depression left left
RIO elevation left right
RLR _ right _
RMR _ left _
45. Muscle
paralysed
chin Face turn Head tilt
LSR elevation left right
LIR depression left right
LSO depression right right
LIO elevation right right
LLR _ left _
LMR _ right _
46. EASY STEPS
1. Know the action of the muscle
2. Know the position of the eye
3. Know what should the head and chin do to keep
the eye in that position or to make the eye more
tropic(or other reasons discussed earlier)
53. Left SO palsy,head
turn with tilt in right
side
Upshoot of LE due
to contracture of
LIO
Parallelism of
visual axes in
laevo-version
54. LIR
PALSY ACTION OF IR
MUSCLE
EYE POSITION
ELEVATED
INTORTED
ABDUCTED
CHIN
DOWN
HEAD
TILT TO
RIGHT
FACE
TURN TO
LEFT
55. Compensatory head posture
in RIR ,face turn to
right,head tilt to left and
chin depressed
Dextroversion
showing depression
of left eye
Dextrodepression,
defective
movement of RE
with overaction of
LSO
56. RSR
PALSY
ACTION OF SR
MUSCLE
EYE POSITION
DEPRESSED
ABDUCTED
EXTORTED
FACE
TURN TO
RIGHT CHIN
UP
HEAD
TILT TO
RIGHT
57. FIXING WITH NORMAL EYE
FIXING WITH PARETIC
EYE
RSR palsy, chin elevation, head tilt to
right with face turn to right(common
occurrence)
RSR palsy, head tilt and face turn
to the left (less common
occurrence)
58. In primary
position without
head posture,LE
hypotropic
In
dextroversion
,parallelism of
visual axes
Updrift of
right eye in
laevoversion
Congenital
paresis of left
superior rectus,
motor adapted
condition
59. LIO
PALSY ACTION OF IO
MUSCLE
EYE POSITION
INTORTED
ADDUCTED
DEPRESSED
FACE
TURN TO
RIGHT
HEAD
TILT TO
LEFT
CHIN UP
61. Mnemonics for head turn and tilt in superior
rectus and superior oblique palsy
SO U RS
SUPERIOR OBLIQUE SAME SIDE
UNAFFECTED
SIDE sUPERIOR RECTUS
THIS HEAD POSTURE IS ADAPTED TO MAINTAIN BSV
LEFT SO PALSY
LEFT SR
PALSY
62. ISOLATED VARIETIES OF OCULAR PALSY
Most common muscles to be paralysed singly :
superior oblique and lateral rectus
WHY ? ?
BECAUSE
THEY HAVE
SEPARATE
NERVE
SUPPLY
63. In case of MR, IO, SR and IR
Supplied by 3rd cranial nerve, less likely to occur isolated
muscle palsy…
total 3rd nerve palsy
3rd nerve palsy
partial 3rd nerve palsy
Note: in both cases pupil may or may not be spared
in total palsy : both division involved
in partial : only one division involved
in isolated muscle palsy : only one muscle involved
64. TOTAL 3RD NERVE PALSY
Extraocular (IR, MR, IO and SR) , LPS muscle as
well as intraocular muscle (sphincter pupillae and
ciliary muscle) affected
Dilated
pupil
Complete loss
of
accomodation
ptosis
65. MOTOR ADAPTATION IN TOTAL 3RD NERVE
PALSY
Occcurs only if pupil is spared so that the patient
experience diplopia requires adaptation
Eye is turned down ,out and slightly intorted
SLIGHTLY
CHIN UP FACE TURN
TOWARDS
OPPOSITE
SIDE
HEAD TILT
TO SAME
SIDE
66. PARTIAL 3RD NERVE PALSY
SUPERIOR DIVISION
PALSY :
-SR and LPS muscle
involved
-ptosis with hypotropic
eye
- Chin elevated , face turn
and head tilt to affected
side
INFERIOR DIVISION
PALSY :
-IR, IO and MR in
addition to sphincter
pupillae and ciliary
muscle involved
-exotropic,intorted and
hypertropic eye with
pupil dilatation
-unlikely to be any field of
binocular vision
-So , no need for AHP
67. Restriction of movement of LE
in all gazes except in abduction
LEFT THIRD NERVE PALSY
Head tilt and face turn to right
with chin up to avioid diplopia
68. DOUBLE ELEVATOR PALSY
Aka monocular elevation deficiency
paralysis of both elevators of same eye
i.e superior rectus and inferior oblique
elevation deficiency in entire upgaze i.e
both upward adduction and abduction
69. Head posture
Eyes made more hypotropic by doll’s head
phenomenon i.e chin is elevated
70. DOUBLE DEPRESSOR PALSY
Aka monocular depression deficiency
both depressors of same eye i.e inferior rectus and
superior oblique are paralysed
depression deficiency in entire downgaze both in
adduction and abduction
71.
72. Head posture
Eyes made more hypertropic by doll’s head
phenomenon i.e chin is depressed
73. SPECIAL RESTRICTIVE DISORDERS
Disorders that are non –paralytic but restricts the
ocular movement
Caused by elements within orbit that either interfere
with muscle contraction or relaxation or otherwise
prevent free movement of globe
75. DUANE’S RETRACTION SYNDROME
there is fibrosis or inelasticity of the lateral rectus
muscles and that the medial rectus muscle inserts
abnormally far posteriorly myogenic cause
absent abducens nerve with anomalous innervations
of the lateral rectus muscle by a branch of the
oculomotor nerve,
Simultaneous activation of the medial and
lateral rectus muscles the cause of globe
(neurogenic ) retraction
there is fibrosis or inelasticity of the lateral rectus
muscles and that the medial rectus muscle inserts
abnormally far posteriorly myogenic cause
absent abducens nerve with anomalous innervations
of the lateral rectus muscle by a branch of the
oculomotor nerve,
Simultaneous activation of the medial and
lateral rectus muscles the cause of globe
(neurogenic ) retraction
76. AHP in DRS
Adopted to centralize BSV
Determined by deviation in primary posistion
ESOTROPIC : face turn to affected side
EXOTROPIC : face turn to unaffected side
77. TYPE I DRS
Marked limitation of
abduction
Normal or slightly
defective adduction
Narrowing of PFH on
adduction
Widening of PFH on
abduction
78. TYPE II DRS
Marked limitation
of adduction
Normal or slightly
defective abduction
Narrowing of PFH
on adduction
79. DUANE’S RETRACTION SYNDROME,TYPE II
Head posture to
compensate for left
medial rectus paresis
Dextroversion ,
defective adduction of
LE and narrowing of
PFH of LE
Laevo version,
parallelism of
visual axis, slight
widening of left
PFH
80. TYPE III DRS
Marked limitation
of adduction and
abduction
Narrowing of PFH
on adduction and
abduction
81. BROWN’S SYNDROME
Aka superior oblique tendon sheath syndrome
Apparent/pseudo paralysis of inferior oblique
muscle, limitation of elevation in adduction
Due to restriction of IO action by an overly taut
superior oblique tendon of the same eye
Widening of PFH on adduction
Few may have in primary position
responsible for head posture
hypotropia
82.
83. AHP in BROWN’S SYNDROME
Head tilt to affected side
Face turn to contralateral side
Chin elevation
head posture confined to chin elevation if
syndrome is bilateral
84. GRAVE’S OPHTHALMOPATHY
May be associated with hyper, hypo or euthyroidism
Circulating thyroglobulins, and anti thyroglobulin
immune complex bind to EOM ophthalmopathy
in sequence of I’M SLOW
Inferior rectus
Medial rectus
Superior
rectus
Lateral rectus
Oblique muscles
85. Common ocular mobility defect is U/L elevator
deficiency followed by defective abduction
eye is hypotropic and esotropic
Chin
elevation
with or
without Face
turn to same
side
86.
87. FIBROSIS OF EOMs
Group of congenital anomalies with restrictions of
EOMs
Due to replacement of muscle fibres by the fibrous
tissue
Ranges from isolated fibrosis to B/L involvement of
all EOMs
88. GENERALIZED FIBROSIS SYNDROME
Fibrosis of all EOMs
no elevation or depression
little or no horizontal movement
Bilateral ptosis
AHP : backward head tilt with chin elevated
89. STRABISMUS FIXUS
Rare disorder , commonly with marked esotropia
associated with extreme tightness of MR muscle
Most patient adopt chin elevation
91. A-PATTERN HETEROTROPIA
Increasing convergence in upgaze and increasing
divergence in downgaze
For A-pattern esotropes,to make eyes relatively
convergent in downgaze,the chin is elevated
For A-pattern exotropes,to make eyes relatively
divergent in upgaze,the chin is depressed
92.
93. V-PATTERN HETEROTROPIA
Increasing convergence in downgaze and increasing
divergence in upgaze
For V-pattern exotropes,to make eyes relatively
convergent in upgaze,the chin is elevated
For V-pattern esotropes,to make eyes relatively
divergent in downgaze,the chin is depressed
94.
95. INFANTILE ESOTROPIA
Manifest eso deviation with an onset between birth
and 6 months of age
Etiology unknown
Head & face tilt towards the shoulder of the fixating
eye
In some cases AHP associated with ML nystagmus
Pt turn head towards the side of the fixing eyewhich gets
optimal visual acuity in the position of adduction
96. Congenital esotropia with
manifest nystagmus,
left eye fixing in
adduction, head turned
towards left, the direction
of the left fixing eye ; pre
op
Post-op picture after bi-
lateral medial rectus
recession
no head turn