Paralytic strabismus

1. Paralytic strabismus
lMovement of the eye, following contracture
of a muscle can be considered in terms of
the action of an individual, isolated muscle

3. this does not aid in the diagnosis of the
affected muscle in paretic situation.
lthe field of action of the muscle should be
considered
lThis is the direction in which the muscle’s
primary position action has maximal effect.

6. Terms
lAgonist = prime mover or protagonist
lAntagonist= muscle having the opposed
action
lSynergist = muscle having the same actions
lIpsilateral = on the same side
lContralateral = on the opposite side
lContracture = increased resistance against
passive stretching of the muscle, loss of
elasticity

7. Hering’s Law of Equal
Innervation
lequal and simultaneous innervation flows to the synergistic
muscles concerned with the desired direction of gaze
(applies to voluntary and involuntary eye movements)
lie innervation of one eye is equal that of the other eye,
resulting in movements of the two eyes that are equal
symmetrical and parallel (normally)
lThis law has great practical significance when used in the
diagnosis of paralytic strabismus

8. Sheringtons Law of Reciprocal
Innervation
lconcerned with the co-ordination of muscle
pairs of one eye.
lMuscle contraction does not increase
simultaneously in opposed muscles
lie the contraction of each ocular muscle is
accompanied by a simultaneous and
proportional relaxation of its antagonist.

9. Sequelae of Ocular Muscle
Palsy
lUnderaction of the primary affected muscle
lOveraction of the contralateral synergist
lOveraction of the ipsilateral (direct) antagonist
lUnderaction of the antagonist of the
contralateral synergist (contalateral antagonist)
lOveraction of the ipsilateral synergist??

10. Overaction of the contralateral
synergist
lalways present.
lThis overaction occurs when the affected
eye is fixing as a result of increased
innervation being required to rotate the
affected muscle into its field of action.
lDue to Herings Law an overstimulation of
the contralateral synergist follows
lThis is always the largest overaction in the
sequelae.

11. Overaction of the ipsilateral
(direct) antagonist
lcan lead to a permanent contracture of the
muscle and a loss of elasticity
lIf the patient fixes with the non-involved
eye within a few days a contracture will
develop in the direct antagonist muscle
lbecause the normal contracture of the direct
antagonist is unopposed by the weak
muscle.

12. Underaction of the antagonist of the
contralateral synergist (contalateral
antagonist)
lwith the involved eye fixing, the movement
of the eye into the field of action of the
weak muscles antagonist requires less
innervation than normal due to the
contracture.
lTherefore less innervation is supplied to the
contralateral antagonist which under-acts.

13. Overaction of the ipsilateral synergist
lDuke Elder, 1947

14. For example in paralysis of the
right superior rectus
lunderaction of right superior rectus
loveraction of the left inferior oblique
loveraction of the right inferior rectus
lunderaction of the left superior oblique
l(overaction of the right inferior oblique)

15. ANATOMICAL
CONSIDERATIONS
lThere are 6 extraocular muscles – 4 rectus muscles, 2 oblique muscles
lLength of each @ 40 mm, the inferior oblique being slightly shorter
l5 muscles arise from the apex of the orbit, the inferior oblique arises
form the inferonasal angle of the orbit
lThe 4 recti muscles originate form the apex of the orbit at the level of
the Annulus of Zinn
lThe recti muscles are inserted in front of the ocular equator, the
obliques are inserted behind
lMovements occur about 3 primary axes around the centre of rotation –
the vertical, horizontal and saggital axes
lThe action of a muscle depends on the angle of its plane and the
anterio-posterior axis of the eye. It follows that the action of the muscle
may vary according the positions of the globe in the orbit.

16. Medial Rectus

17. Lateral Rectus : abduction

18. Superior Rectus
lIn the primary position the muscle plane of the SR forms an
angle of 23°with the optical axis.
lIn this position the SR elevates the globe.
lSecondary actions are intorsion and adduction.
lAs the eye moves in adduction the SR is now a greater
adductor and intortor
lIn 67° adduction the SR is exclusively an intortor.
lIn 23° abduction the SR is a complete elevator. The muscle
plane coincides with the optical axis.

19. In primary position muscle plane
of the SR forms angle 23°with
optical axis. In this position SR
Elevates the globe. Secondary
Actions intorsion and adduction

21. In 23° abduction, SR complete
Elevator, muscle plane
coincides with optical axis

22. Superior Oblique
lEye in the primary position, the muscle plane SO forms an
angle of 54° with the optical axis.
lThe primary action is intorsion
lThe secondary action is abduction and depression.
lWhen the eye is adducted 54° the optical axis and muscle
plane coincide and the SO is a pure depressor.
lIn abduction the SO is primarily an intortor.

23. Eye in primary position
Muscle plane SO forms
angle 54° with optical
axis. Action is intorsion
Secondary actions
abduction and depression
RE

24. When globe adducted 54°,
Optical axis and muscle
plane coincide, SO is pure
depressor
RE

25. RE
In abduction SO
is primarily an intortor

26. Inferior Rectus
lWith the eye in the primary position the IR forms an angle
of 23° with the optical axis.
l Thus the relationship is the same as the SR except that it is
an inferior rectus and therefore depresses the eye
lSecondary actions = extortion and adduction.
lAs adduction increases the depressor ability decreases and
extortion increases.
lIn 67° abduction IR = exclusively extortor
lIn 23° abduction IR = exclusively a depressor

27. Inferior Oblique
lWhen the eye is in the primary position, the muscle plane
of the IO forms an angle of 51° with the optical axis.
lthe relationship is almost the same as the SO, except by
virtue of the muscles anatomical position, the action is
extorsion.
lSecondary actions are abduction and elevation
lWhen the eye is adducted 51° the muscle is still an extortor
but the elevator action increases
lIn abduction the IO extortion ability increases.

28. Muscle Direct 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
Direct antagonist Muscle
For right eye read from the top
For left eye read from the bottom

29. Rule for the secondary actions of
the vertical muscles
lRADSIN = Recti ADduct Superiors INtort

30. INCOMITANT STRABISMUS
: CLASSIFICATION AND INVESTIGATION
lDefinition:a strabismus where the angle
or degree of the deviation varies in different
directions of gaze OR with each eye fixing
(ie the secondary deviation is greater than
the primary).

31. Classification
lAccording to the underlying cause:
l(i) neurogenic
l(ii) mechanical
l(iii) myogenic
lAlso may be congenital or acquired

32. Congenital
lUsually isolated defects in otherwise healthy individuals
lSometimes familial
lSpecific cause unknown, presumed due to a developmental
anomaly in the anatomy or functioning of the extra-ocular
muscles or their innervating nerves
lSome are associated with serious developmental
neurological defects eg hydrocephalus & cerebral palsy
lGradually become more comitant as Px gets older
lNot likely to respond to orthoptic treatment

33. Acquired
lCaused by injury or disease of the ocular
motor system eg trauma, inflammation,
lVascular
lSpace-occupying lesions
lMetabolic disorders
lNB It is vital that we distinguish between
longstanding/ static acquired disorders and
recent onset/active ones

34. INVESTIGATION OF
INCOMITANCY
lHistory and Symptoms
lGeneral observation of the patient
lCover Test with and without AHP
lMotility
lHess Screen Plots

35. History and Symptoms
lIn general symptoms are likely to be marked and dramatic in recent
onset incomitancy, with the time of onset known.
l In longstanding cases, they are less marked and intermittent due to the
intervention of suppression, and the patient may not complain of
symptoms.
lDiplopia – present in most incomitancy, usually with a vertical
element.
»May only be present in one gaze direction.
»May be intermittent in longstanding cases.
»Establish type, gaze direction, constant/intermittent, associated
symptoms, with or without Rx, diurnal variation, onset, any change
since onset, previous history of diplopia, compensating factors,
how troublesome.

36. History and Symptoms
lAbnormal head posture – patient more likely to be aware of
this in recent onset.
lBlurred vision
lDifference in pupil size
lOther symptoms due to underlying disease (eg HA,
malaise, weight loss, appetite changes, fatigue, muscle
tremor etc)
lInjury to head or orbital regions may be reported – not
necessarily recent.
lIncludes during birth delivery (eg forceps) and surgical
trauma (eg strabismus surgery)

37. General observation of the
patient
lNote the presence of the following:

38. Abnormal head posture
lPurposes
l(I) to place the eyes in the position of least
deviation to enable BSV
l(ii) to centralise the field of BSV
l(iii) to avoid direction of gaze where there is
discomfort or pain
l(iv) occasionally to separate diplopic images
widely (atypical)

39. Components
lFace turn – to the left or right.
lChin elevation or depression
lHead tilt – occurs for two reasons

40. Face turn – to the left or right.
lThis can indicate an anomaly of the medial
rectus or lateral rectus muscle
lPlaces the eyes away from the direction of
the underaction & into the position of the
least deviation ie turn towards affected
muscle.

41. Chin elevation or depression
lto place the eyes in position of least
deviation eg in A and V syndromes
l to avoid discomfort eg chin is often
elevated in Pxs with dysthyroid eye disease,
who can find it uncomfortable to look up.
lAlso in Browns syndrome.

42. Head tilt : occurs for 2 reasons
lin vertical deviations (without cyclotropia)) to level up the
diplopic images
lIn cyclotropia (mainly a function of the obliques) eg SO
palsy results in excyclotropia due to loss of intorting effect,
hence tilt away from affected side so does not have to intort
lIO palsy results in incyclotropia; head tilt towards affected
side.

43. Head tilt : occurs for 2 reasons
lSR and IR palsies: direction of tilt is inconsistent; may be
as result of overaction of the contralateral synergic muscle
rather than primary affected muscle
lHead tilt may be combined with face turn and chin
elevation/depression
l AHP is less obvious in longstanding deviations due to
increased comitancy and suppression.
lAbsence of AHP does not mean absence of incomitancy.
lAHP may remain due to habit.

44. Cover Test with and without
AHP

45. Cover Test: comparison of
deviation with each eye fixing
lprimary deviation = non strabismic eye fixing
lSecondary deviation = strabismic eye fixing
lThe detection of a larger movement in one eye than the
other helps to identify the weak member of the yoke
muscle pair.
lDue to Hering’s Law of equal innervation when one eye is
covered the fixing eye will determine the amount of
innervation transmitted to both eyes
lExcessive innervation is required to move and maintain the
eye in the primary position

46. Cover Test: comparison of
deviation with each eye fixing
lThe same amount of innervation flows simultaneously to
the yoke muscle in the sound eye and the angle of deviation
is larger when the patient uses the eye with the weak
muscle for fixation than when the patient fixates with the
sound eye.

47. Motility – check
lBoth eyes move smoothly and follow the target across the
horizontal, and there is no narrowing of the palpebral
apertures
lThere is a corresponding lid movement accompanying the
vertical movements, and there is no A and V pattern
lThere is no restriction of the movement of the eye in any
direction of gaze
lAid detection of incomitancy by: asking for subjective
doubling
lObserving corneal reflexes

48. Motility – check
lObserving symmetry of lid positions
lUsing red/green diplopia goggles
lCombining with cover test in different positions of gaze
lMeasure the degree of incomitancy by : PCT
lMaddox Rod
lHess screen methods
lPast Pointing – due to a disturbance of absolute localisation

49. 3 step technique
(more reliable in fairly recent paresis)
lRight Hypertropia
lEither RSO, RIR, LSR, LIO underacting

50. 3 step technique
(more reliable in fairly recent paresis)
lR Hypertropia greater in dextroversion
lEither RIR, LIO underacting

51. 3 step technique
(more reliable in fairly recent paresis)
lR Hypertropia greater in levoversion
lEither RSO, LSR underacting

52. 3 step technique
(more reliable in fairly recent paresis)
lTilt head to right shoulder
lRE central, LE depressed = LIO

53. 3 step technique
(more reliable in fairly recent paresis)
lTilt head to left shoulder
lLE central, RE elevated = RIR

54. 3 step technique
(more reliable in fairly recent paresis)
lHas the patient got a right or left hypertropia?
lIs the hypertropia greater in right or left gaze?
lIs the hypertropia greater with a head tilt to the right or
left?
lBased on Bielschowsky head tilt test (next week)

55. Hess Screen Plots
lCompare the size of the fields
lthe affected eye corresponds to the smaller field – the involved eye
shows the greatest under-action and smallest over-action compared
with the non-involved eye
lGreater difference in size will be found in mechanical or recent onset
neurogenic deviations
lIn longstanding neurogenic defects the full sequelae is present – spread
of incomitance = smaller difference in plots between eyes
lMechanical vs Paralytic Strabismus
lMechanical (and recent onset palsy) only shows first and second parts
of the sequelae
lMechanical deviations failure is more abrupt – making the defect small
in the central field in comparison to the outer field

56. Lateral Rectus
lGreatest defect occurs on attempts to abduct
the paretic eye
lUsually esotropia in the primary position
lHead turn towards palsied side

57. Medial rectus
lIsolated paresis is rare
lGreatest defect occurs when palsied eye
adducts
lUsually exotropia in primary position
lHead turn is towards sound side

58. Superior Rectus
lIsolated palsy is usually congenital
lParetic eye is affected in elevation and abduction
lElevation is limited in the primary position, but normal on
adduction
lParetic eye is hypotropic in the primary position
lFrequent torticollis, but not of good diagnostic value (head
held up and top palsied side or tilting of head to the paretic
side)
lUsually associated with weakness of the levator (psuedo-
ptosis – usually disappears when the paretic eye fixates)
lContralateral inferior oblique will overact

59. Inferior Rectus
lIsolated palsy is rare and usually congenital
lGreatest deviation on attempts to look downward with the
paretic eye in abduction
lUnopposed antagonist (SR) causes the paretic eye to be
incyclotropic and hypertropic in the primary position
lPseudoptosis in the sound eye
lHead turns down and to the paretic side with tilt to the
sound side

60. Inferior Oblique
lLeast likely of the muscles innervated by the 3
rd
cranial
nerve to be paralysed
lGreatest deviation when the patient attempts to elevate the
adducted eye
lOveraction of the unopposed antagonist (SO) causes
incyclotropia
lNearly always congenital
lHead posture is fairly characteristic with head inclined
towards the paretic side and face turned towards the sound
side
lOften confused with Browns Tendon Sheath Syndrome

61. Superior Oblique
lGreatest defect with the eye adducting in depression
lOveraction of the antagonist inferior oblique causes the
paretic eye to be hypertropic in the primary position
lOften secondary contracture of the IO occurs to a large
degree so that it appears as the most prominent sign
lHead position is characteristically tilted towards the
uninvolved side and the chin is depressed