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366 Theory and Practice of Squint and Orthoptics
• Emphysema of the eyelids occurs more
frequently with medial wall than floor
fractures. It may be made worse by blowing
of nose. Paraesthesia and anaesthesia in
infraorbital nerve distribution (lower lid,
cheek, side of nose, upper lip and upper teeth)
are very common.
• Ipsilateral epistaxis as a result of bleeding from
maxillary sinus into the nose is frequently
noted in early stages. Proptosis of variable
degree may also be present initially because
of the associated orbital oedema and
haemorrhage.
• Enophthalmos. After about 10 days, as the
oedema decreases, the eyeball sinks backward
and somewhat inferiorly resulting in
enophthalmos. Three factors responsible for
producing enophthalmos are: (a) escape of
orbital fat into the maxillary sinus; (b)
backward traction on the globe by entrapped
inferior rectus muscle and (c) enlargement of
the orbital cavity from displacement of
fragments.
• Diplopia also becomes evident after decrease
in oedema. It typically occurs in both up- and
downgaze (double diplopia) due to
entrapment of soft tissue structures in the area
of the blow-out fracture (floor more
commonly than medial wall).
The presence of muscle restriction can be
confirmed by a positive 'forced duction test'.
• Restricted elevation, restricted depression may
occur in fracture floor of the orbit.
• Pseduo-Duane's refraction syndrome (or acquired
inverse-Duane's syndrome), presentation may
occur in fracture of medial wall of the orbit.
• Saccadic eye movement testing is sometimes
helpful to determine whether ocular
movement limitation is because of a restrictive
process or a paretic process.
• Associated severe ocular damage is rare. This is
because a 'blow-out fracture' is nature's way of
protecting the globe from injury. Nevertheless
the eye should be carefully examined to exclude
the possibility of intraocular damage.
(Water's) view. The common radiological
findings are—fragmentation and irregularity of
the orbital floor; depression of bony fragments
and 'hanging drop' opacity of the superior
maxillary antrum from orbital contents
herniating through the floor (Fig. 12.53).
2. Computerised tomography scanning and
magnetic resonance imaging. These are of
greater value for detailed visualisation of soft
tissues. Coronal sections are particularly useful
in evaluating the extent of the fracture.
Management
Surgical repair to restore continuity of the orbital
floor may be made with or without implants.
It may not be required in many cases.
• Optimal time for surgery, when indicated, is
after 10–14 days of injury.
• Indications of surgical intervention include:
– Diplopia not resolving significantly in the
early days after trauma
– A fracture with a large herniation of tissues
into the antrum
– Incarceration of tissues in the fracture with
resulting globe retraction and increased
applanation tension on attempted upward
gaze; and
– Enophthalmos greater than 3 mm.
Any of these factors, alone or combined, could
indicate that early orbital repair is necessary.
Radiological examination
1. Plain X-rays. The most useful projection for
detecting an orbital floor fracture is a nose-chin
Fig. 12.53 Plain X-ray orbit (AP view) showing herniated
orbital contents (arrow) with blow-out fracture of the orbital
floor.
Incomitant Strabismus
367
Residual strabismus after 3–6 months of injury
can generally be corrected by using standard
eye muscle surgical techniques:
• Recession of inferior is done first
• Resection of superior rectus may also be done,
if required.
STRABISMUS FIXUS
In strabismus fixus, fibrosis involves the
horizontal recti and the involved eye is fixed in
extreme position. It may be unilateral or
bilateral. It occurs in two forms—convergent
and divergent.
Strabismus fixus convergence is more common.
Etiology. Strabismus fixus convergence (SFC)
can be congenital or acquired.
• Congenital cases are more common. In such
cases, lateral rectus palsy with medial rectus
fibrosis has been described as the cause.
• Acquired cases though rare, are reported to be
due to myopic myositis and amyloidosis of the
lateral rectus muscle.
Clinical features Patient's eyes are fixed in
extreme convergent position and he/she cannot
abduct either eye past the midline (Fig. 12.54).
It can be differentiated by forced duction test
from bilateral sixth nerve palsy.
Treatment of strabismus fixus convergence
includes:
• Medial rectus recession. Supramaximal
recession with silicon expanders have been
reported to give good functional and cosmetic
results.
• Loop myopaxy of LR and SR to the sclera in
superotemporal part with non-absorbable
suture or silicon sling is also reported to give
reasonable good results in cases with tight
MR.
• Disinsertion of MR and resection of LR has also
been described.
In addition, recession of the medial conjunctiva
and Tenon's capsule may be needed to bring the
eyes in the centre in primary position.
Strabismus fixus divergence is comparatively
rare condition characterized by fixation of eyes
in extreme divergence.
Surgery for divergent strabismus fixus is just
reverse of the strabismus fixus convergence.
CONGENITAL TIGHT INFERIOR RECTUS MUSCLE
• In some children, a congenital hypotropia
occurs accompanied by marked limitation of
upgaze.
• The condition may be unilateral or bilateral
and in some cases there may be fibrosis of the
levator muscle as well. Probably, the condition
is a variant of generalized fibrosis.
Fig. 12.54 Strabismus fixus convergence
368 Theory and Practice of Squint and Orthoptics
• Forced duction test reveals an inferior
restriction.
• Surgical exploration reveals a tight inferior
rectus which is adherent to the globe.
• Treatment consists of release of globe adhe-
sions and a maximal inferior rectus
recession, to relieve the restriction in upward
rotation.
STRUCTURAL ADHESIONS
ADHERENCE SYNDROME
Clinical features. Two types of adherence
syndrome, the lateral adherence syndrome and
superior adherence syndrome, have been
reported to occur due to developmental
abnormal fascial connections.
• In the lateral adherence syndrome, an abnormal
fascial connection is seen between the muscle
capsule of the lateral rectus and inferior
oblique, which produces limitation of ocular
rotation in the field of lateral rectus muscle.
• In the superior adherence syndrome, an
abnormal fascial connection exists between
the superior rectus and tendon of the superior
oblique, causing limitation of rotation in the
field of superior rectus muscle.
Treatment consists of severing of all the
adhesions after disinsertion of the lateral or
superior rectus muscle. To confirm that, all the
adhesions have been removed, after the surgery,
eye should be rotated medially for lateral
adherence syndrome and inferiorly for superior
adherence syndrome.
TIGHT LATERAL RECTUS SYNDROME
Causes. This syndrome is probably seen most
commonly in association with a long-standing
large angle exotropia. Large bimedial recession
followed by contracture of the lateral recti has
also been implicated as a cause.
Clinical features. The tight lateral rectus
syndrome is characterized by bilateral restriction
of the eyes on attempted adduction and an
apparent overaction of all the four obliques.
• Forced duction test shows restriction of both the
lateral recti, an observation which helps in
differentiating it from bonafide oblique overaction.
Treatment consists of recessions of the lateral
recti combined with temporal conjunctival
recession. Medial rectus, resection or advancement
may be required.
CONTRACTURE OF EXTRAOCULAR MUSCLES
• Contracture of antagonist extraocular muscle is
of common occurrence after paralysis of an
agonist extraocular muscle, that with time
produces a restriction.
• Treatment consists of recessing the antagonist
muscle.
ADHESIVE SYNDROME
• Adhesive syndrome or cicatricial strabismus
refers to a restrictive type of strabismus
which occurs following squint surgery, most
commonly after inferior oblique myectomy
done at the insertion end of the muscle.
• It is thought to result from a fibrous and fatty
proliferative inflammatory response following
surgical entry of the portion of Tenon's capsule
and fat into the wound.
• Hypotropia is associated with an inferior
restriction or forced duction test.
POSTOPERATIVE SCARRING
Postoperative scarring of the conjunctiva and
extraocular muscles may occur producing
restrictions. Treatment consists of recession of
the affected muscles and conjunctiva.
Postoperative scarring of the Tenon's capsule
has been reported to produce an L-deformity of
inferior oblique, J-deformity of rectus muscle
and cicatricial advancement of a rectus muscle.
• L-deformity of the inferior oblique occurs
following accidental incorporation of the
inferior oblique into the insertion of lateral
rectus muscle during resection surgery on it.
• J-deformity of a rectus muscle refers to
postoperative pull of the belly of the
recessed muscle forward over the insertion
site. It occurs due to the 'purse-string' pulling
action of Tenon's capsule following an
insufficient surgery on it.
• Cicatricial advancement of a rectus muscle also
results from an insufficient surgery on the
intermuscular membrane and Tenon's
Incomitant Strabismus
369
capsule. The 'purse-string' action of the
insufficiently separated Tenon's capsule pulls
the new insertion of the muscle back to its
original insertion.
Treatment consists of re-exploration to define
the problem and release the restriction.
ORBITAL MYOSITIS
Causes: The clinical spectrum of orbital myositis
can be seen in the following conditions:
• Idiopathic orbital inflammatory disease (IOID)
• Autoimmune myositis
• Cysticercosis of extraocular muscles
• Mild grade orbital cellulitis.
Clinical features include:
• Ocular pain
• Conjunctival congestion
• Proptosis
• Ptosis may also occur in some cases
• Deviation of the involved eye and diplopia
• Restriction of eye movements (positive forced
duction test).
Investigations helpful in diagnosis include:
• Orbital ultrasonography
• CT scan/MRI imaging of the orbit and head
(to rule out suspected neurocysticercosis).
Treatment
• Systemic steroids are useful in idiopathic orbital
inflammatory diseases and autoimmune
myositis.
• Oral albendazole, under cover of steroids is
useful in cysticercosis.
• Antibiotics and anti-inflammatory drugs are
needed in mild grade orbital cellulitis.
BIBLIOGRAPHY
1. Adler FH: Superior oblique tendon sheath
syndrome of Brown. Arch. Ophthalmol. 48:264,
1959.
2. Aebli R: Retraction syndrome. Arch. Ophthalmol.
10:602, 1933.
3. Afifi AK Bell. WE, and Menezes, AH: Etiology
of lateral rectus palsy in infancy and childhood
J Child. Neurol, 7:295, 1992.
4. Ahluwalia BK, Gupta NC, Goel SR and Khurana,
AK: Study of Duane's retraction syndrome.
Acta Ophthalmol. 66:728, 1988.
5. Albert DG: Personal communication. In Parks,
MM: Annual review: strabismus. Arch.
Ophthalmol. 58:152, 1957.
6. Arimoto H: Ocular findings of thalidomide
embryopathy. Jpn J Clin Ophthalmol. 33:501,
1979.
7. Bahn RS and Heufelder, AE: Pathogenesis of
Graves ophthalmopathy. N Engl J Med 329:1468,
1993.
8. Bell JA, Fielder AR and Viney S: Congenital
double elevator palsy in identical twins. J Clin
Neuro Ophthalmol. 10:32, 1990.
9. Berens C and Girard, L: Transplantation of the
superior and inferior rectus muscles for
paralysis of the lateral rectus muscle. Am J
Ophthalmol. 33:1041, 1950.
10. Berlit P: Isolated and combined pareses of
cranial nerves III, IV and VI. A retrospective
study of 412 patients. J. Neurol. Sci. 103:10,
1991.
11. Bielschowsky, A:2 Die Motilitatsstorungen der
Augen. In Axenfeld, T, and Elschnig, A, editors:
Graefe Saemisch's Handbuch der gesamten
Augenheikunde, ed. 2, vol. 8, Berlin, 1939,
Julius Springer.
12. Bielschowsky A: Lectures on motor anomalies,
Hanover, NH, 1943 (reprinted 1956). Dartmouth
College Publications.
13. Boyd. TAS, Leitch, GT, and Budd, GE: A new
treatment for "A" and "V" patterns in strabismus
by slanting muscle insertions: a preliminary report.
Can. J Ophthalmol. 6: 170, 1971.
14. Breinin G: The physiopathology of the A- and
V-patterns. In Symposium: the A- and V-patterns
in strabismus. Trans Am Acad Ophthalmol.
Otolaryngol. 57:157, 1953.
15. Brosky MC, Pollock SC and Buckley EG: Neural
misdirection in congenital ocular fibrosis
syndrome: Implications and pathogenesis. J
Pediatr. Ophthalmol, Strabismus 26:159, 1989.
16. Brown HW: Congenital structural muscle
anomalies. In Allen, JH, editor: Strabismus
ophthalmic symposium I. St. Louis, 1950,
Mosby- Year Book. Inc., p. 205.
17. Brown HW: Isolated inferior oblique paralysis.
Analysis of 97 cases. Trans. Am. Ophthalmol.
Soc, 55:415, 1957.
18. Brown HWL: Congenital structural anomalies
of the muscles. In Allen, JH editor: Strabismus
ophthalmic symposium II, St. Louis, 1958,
Mosby-Year Book, Inc., p. 391.
19. Brown HW: True and simulated superior oblique
tendon sheath syndromes. Doc. Ophthalmol.
34: 123, 1973.
370 Theory and Practice of Squint and Orthoptics
20. Brown HW: Vertical deviations. In Symposium,
strabismus. Trans. Am. Acad Ophthalmol.
Otolaryngol. 57:157, 1953.
21. Brown WB: Isolated inferior oblique paralysis.
Trans Am. Ophthalmol. Soc. 55:415, 1957.
22. Burke JP, Ruben JB and Scott WE: Vertical
transposition of the horizontal recti (Knapp
procedure) for the treatment of double elevator
palsy: effectiveness and long-term stability. Br.
J Ophthalmol. 76:734, 1992.
23. Burian HM and Van Allen MW: Cyclic oculomotor
paralysis. Am. J Ophthalmol. 55:529, 1963.
24. Costenbader FD: Introduction. In Symposium:
the A- and V-patterns in strabismus. Trans. Am.
Acad. Ophthalmol. Otolaryngol. 68:354, 1964.
25. Dotti MT, Federico A, Palmeri S, and Guazzi
GC: Congenital oculo-facial paralysis (Moebius
syndrome) evidence of dominant inhertance in
two families. Acta Neurol. 11:434, 1989.
26. Duane A: Congenital deficiency of abduction
associated with impairment of adduction,
retraction movements, contraction of the
palpebral fissure and oblique movements of
the eye. Arch. Ophthalmol. 34:133, 1905.
27. Duane RD, Schatz NJ and Caputo AR: Pseudo
Duane's retraction syndrome. Trans. Am.
Ophthalmol. Soc. 74:122, 1976.
28. Duke-Elder S and Wybar K: System of
ophthalmology, vol. 6: Ocular motility and
strabismus, St. Louis, 1973, Mosby-year Book,
Inc., p. 736 ff.
29. Esswein MB and Noorden GK von: Paresis of
a vertical rectus muscle after cataract surgery.
Am J Ophthalmol. 116:424, 1993.
30. Fells P and Collin JRO: Cyclic oculomotor palsy.
Trans. Ophthalmol. Soc. UK 99:192, 1979.
31. Fink WH: The A and V syndromes. Am.
Orthopt. J. 9:105, 1959.
32. Fitzsimmons R, Lee J and Elston J: The role of
botulinum in the management of sixth nerve
palsy. Eye 3:391, 1989.
33. Fitzsimmons R, Lee JP and Elston J: Treatment
of sixth nerve palsy in adults with combined
botulinum toxin chemodenervation and surgery.
Ophthalmology 95:1535, 1988.
34. Gobin MH: Sagittalization of the oblique
muscles as possible cause for the "A", "V", and
"X" phenomena. Br J Ophthalmol. 52:13, 1968.
35. Gopal KSS: Acquired double depressor palsy.
Indian J. Ophthalmol. 36:35, 1988.
36. Gottlob L, Catalano RA and Reinecke RD:
Surgical management of oculomotor nerve
palsy. Am J Ophthalmol. 111:71, 1991.
37. Guyton D: Exaggerated traction test for the
oblique muscles. Ophthalmology 88:1035, 1981.
38. Hardesty HH: Diagnosis of paretic vertical
rotators. Am.JOphthalmol. 56:811, 1963.
39. Helveston EM: A new two step method for the
diagnosis of isolated cyclovertical muscle
palsies. Am. J. Ophthalmol. 64:914, 1967.
40. Helveston EM, Krach D, Plager DA and Ellis
FD: A new classification of superior oblique
palsy based on congenital variations in the
tendon. Ophthalmology 99:1609, 1992.
41. Huber A: Electrophysiology of the retraction
syndrome. Br J Ophthalmol. 58:293, 1974.
42. Jampolsky A: Oblique muscle surgery of the Aand V-pattern. J Pediatr. Ophthalmol. 2:31,
1965.
43. Jampolsky, A: Surgical leashes and reverse
leashes in strabismus surgical management. In:
Symposium on strabismus: transactions of the
New Orleans Academy of Ophthalmology, St.
Louis, 1978, Mosby-Year Book. Inc., p.244.
44. Khawam E, Scott A and Jampolsky A: Acquired
superior oblique palsy. Diagnosis and
management. Arch. Ophthalmol, 77:761, 1967.
45. Knapp P and Moore S: Diagnosis and surgical
options in superior oblique surgery. Int.
Ophthalmol. Clin. 16:137, 1976.
46. Knapp P: Diagnosis and surgical treatment of
hypertropia, Am, Orthopt. J. 21:29, 1971.
47. Knapp P: Vertically incomitant horizontal
strabismus: the so-called A and V syndrome.
Trans. Am. Ophthalmol. Soc, 57:666, 1959.
48. Knapp P: A- and V-patterns. In Symposium on
strabismus. Transactions of the New Orleans
Academy of Ophthalmology, St. Louis, 1971,
Mosby - Year Book, Inc., p 242.
49. Kodsi SR and Younge BR: Acquired oculomotor, trochlear, and abducent cranial nerve
palsies in pediatric patients. Am. J. Ophthalmol.
114:568. 1992.
50. Manners RM, O'Flynn E and Morris RJ: Superior
oblique lengthening for acquired superior oblique
overaction. Br J Ophthalmol. 78:280, 1994.
51. Metz HS: Saccadic velocity measurements in
strabismus. Trans, Am. Ophthalmol. Soc. 81:630,
1983.
52. Metz HS, Scott AB and Scott WE: Horizontal
saccadic velocities in Duane's syndrome. Am. J.
Ophthalmol. 80:901, 1975.
53. Noorden GK von, Awaya S and Romano PE:
Past-pointing in paralytic strabismus. Am. J
Ophthalmol. 71:27, 1971.
Incomitant Strabismus
371
54. Noorden GK von and Hansell R: Clinical
characteristics and treatment of isolated inferior
rectus paralysis, Ophthalmology 98:253, 1991.
55. Noorden GK von, Murray E and Wong SY:
Superior oblique paralysis. A review of 270
cases. Arch. Ophthalmol. 104:1771, 1986.
56. Noorden GKvon and Ruttum M: Torticollis in
paralysis of the trochlear nerve. Am Orthopt. J
33: 16, 1983.
57. Noorden GK von, Tredici TD and Ruttum M:
Pseudo-internuclear ophthalmoplegia after
surgical paresis of the medial rectus muscle.
Am J Ophthalmol. 98:602, 1984.
58. Noorden GK von and Olson CL: Diagnosis and
surgical management of vertically incomitant
horizontal strabismus. Am J Ophthalmol. 60:434,
1965.
59. Olivier P and Noorden GK and Excyclotropia
of the nonparetic eye in unilateral superior
oblique muscle paralysis. Am. J. Ophthalmol.
93:30, 1982.
60. Olivier P and Noorden GK von: Results of
superior oblique tenectomy in inferior oblique
paresis. Arch. Ophthalmol. 100-581, 1982.
61. Parks MM: Isolated cyclovertical muscle palsy.
Arch. Ophthalmol. 60: 1027, 1958.
62. Parks MM: The weakening surgical procedures
for eliminating overaction of the inferior oblique
muscle. Am J Ophthalmol, 73:107, 1972.
63. Roper-Hall G and Feibel RM: Measurement of
the field of binocular single vision in the
evaluation of incomitant paralytic strabismus.
Am. Orthopt. J 24:77, 1974.
64. Rush JA and Younge BR: Paralysis of cranial
nerves III, IV, and VI: causes and prognosis in
1,000 cases. Arch. Ophthalmol. 99:76, 1981.
65. Ruttam M and Noorden GK von: Orbital and
facial anthropometry in A- and V-pattern
strabismus. In Reinecke, RD, editor: Strabismus
II, New York, 1984, Grune & Stratton, Inc,.,
p. 363.
66. Scott WE and Kraft SP: Classification and surgical
treatment of superior oblique palsies: I.
Unilateral superior oblique palsies. Tran sactions
of the New Orleans Academy of Ophthalmology,
New York, 1986, Raven Press, P. 15.
67. Scott WE and Kraft SP: Classification and surgical
treatment of superior oblique palsies: II. Bilateral
superior oblique palsies. Transactions of the
New Orleans Academy of Ophthalmology, New
York, 1986, Raven Press, p. 265.
68. Scott AB and Stella SL: Measurement of A- and
V-patterns. J. Pediatr. Ophthalmol. 5:181, 1968.
69. Stilling J: Untersuchungen iiber die Entstehung
der Kurzsichtigkeit, Wiesbaden, 1887, J.F.
Bergmann, P. 13.
70. Turk S: Bemerkungen zu einem Falle von
Retraction des Auges. Cbl. Pract. Augenheilk.
23:14, 1899.
71. Urist MJ: Horizontal squint with secondary
vertical deviations. Arch. Ophthalmol. 46:245,
1951.
72. Urist MJ: Recession and upward displacement
of the medial rectus muscles in A-pattern
esotropia. Am J Ophthalmol. 65:769, 1968.
73. Villaseca A: The A and V syndromes. Am. J.
Ophthalmol. 52:172, 1961.
74. Wilson ME and Hoxie J: Facial asymmetry in
superior oblique muscle palsy. J Pediatr.
Ophthalmol. Strabismus 30: 315, 1993.
372 Theory and Practice of Squint and Orthoptics
13
Supranuclear Control and
Disorders of Ocular Motility
SUPRANUCLEAR CONTROL OF EYE MOVEMENTS
Supranuclear ocular motor neural
pathway
Cortical control centres
•
Subcortical control centres
•
Supranuclear eye movement systems
Saccadic system
•
Smooth pursuit system
•
Vergence system
•
Vestibular system
•
SUPRANUCLEAR CONTROL OF
EYE MOVEMENTS
There exists a highly accurate, still not fully
elucidated, supranuclear control of eye
movements which keeps the two eyes yoked
together so that the image of the object of interest
is simultaneously held on both foveas despite
the movements of the perceived object or the
observer’s head and/or body. For the purpose
of understanding, the neural control of eye
movements can be discussed under two parts:
(1) supranuclear ocular motor neural pathway
and (2) supranuclear eye movement systems.
Optokinetic system
•
Position maintenance system
•
SUPRANUCLEAR DISORDERS OF EYE
MOVEMENTS
Ocular motor apraxia
•
Horizontal conjugate gaze paralysis
•
Internuclear ophthalmoplegia
•
One-and-a-half syndrome
•
Vertical conjugate gaze paralysis
•
Skew deviation
•
Cogwheeling
•
Ocular dysmetria, ocular flutters and opsoclonus
•
responsible for controlling the individual eye
muscles. The supranuclear control system is
essential for maintaining accurate and
coordinated eye movements for activities such
as tracking objects, stabilizing gaze, and shifting
attention. Key brain regions involved in the
supranuclear control of eye movements include
(Fig. 13.1):
• Cortical control centres, and
• Subcortical control centres.
CORTICAL CONTROL CENTRES
The cortical control centres include:
• Frontal ocular motor area, and
• Parieto-occipitotemporal (POT) junction.
SUPRANUCLEAR OCULAR MOTOR
NEURAL PATHWAY
Supranuclear control of eye movements refers
to the neural circuits and processes that originate
in higher brain centers and influence the
generation, coordination, and modulation of eye
movements. These brain centers are located
above the level of the cranial nerve nuclei
I. Frontal ocular motor area
The frontal ocular motor area is primarily
involved in the saccadic eye movement system.
It is thought to control voluntary rapid conjugate
gaze, both vertically and horizontally. Recently
four main cortical areas involved in the
generation of saccades have been recognized.
These include: (1) frontal eye field (FEF),
Supranuclear Control and Disorders of Ocular Motility
Fig. 13.1 Showing supranuclear connections of ocular motor neural pathway.
373
(2) supplementary eye field (SEF), (3) dorsolateral prefrontal cortex (DLPFC), and
(4) posterior eye field (PEF).
Frontal eye fields (FEFs) are located at
Brodmann’s area 8, the posterior end of the
second frontal convolution.
Role of the FEF plays a role in generating
voluntary saccadic eye movements. Saccades are
rapid, ballistic movements that shift the eyes
from one point of interest to another. The FEF is
involved in decision-making processes related
to saccades, including selecting the target and
determining the direction and amplitude of the
movement is as below:
• Horizontal gaze movements result, when the
extraocular muscles receive signals from one
hemisphere (contralateral) only. Stimulation
of the frontal lobe area, on the right, for
instance, leads to conjugate movements of
both eyes to the left (Fig. 13.2).
• Voluntary vertical conjugate gaze movements
occur, when equal signals are transmitted
simultaneously from the both frontal ocular
motor areas (Figs 13.3 and 13.4).
Supplementary eye fields (SEF): Also situated in
the frontal cortex, the SEF contributes to the
planning and initiation of voluntary saccades.
It is particularly involved in generating
sequences of saccades, such as those required
for scanning a visual scene.
II. Parieto-occipitotemporal (POT) junction
The ipsilateral parieto-occipital ocular motor
area is primarily concerned with the fixation and
pursuit movements. Following cortical areas
have been identified in relation with the pursuit
movements:
• Middle temporal (MT) visual area, and
• Medial superior temporal (MST) visual area
i. Middle temporal (MT) visual area. The
cerebral cortex in the region of the POT junction
is important in the control of smooth pursuit eye
movements and object tracking in space. This
area is known as the middle temporal (MT) area
in non-human primates. The area of the human
brain that is the equivalent of the MT cortex of
the non-human primate is Flechsig’s area 10. The
MT receives visual information from the striate
and prestriate cortex. It projects to the brainstem,
cerebellum, superior colliculi, and the FEF. The
latter projections modulate visually directed
saccadic eye movements. The POT junction
374 Theory and Practice of Squint and Orthoptics
Fig. 13.2 Pathway for horizontal gaze saccadic eye movements. The horizontal gaze centre (present in PPRF) is
connected with ipsilateral lateral rectus muscle (LR) and with abducens internuclear neurons whose axons cross the
midline and travel in the medial longitudinal fasciculus (MLF) of the opposite side to that part of the nucleus of IIIrd nerve
which innervates the medial rectus muscle.
Supranuclear Control and Disorders of Ocular Motility
375
Fig. 13.3 Pathway for vertical gaze (downgaze) saccadic eye movements.