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Review Article
Surgical management of third nerve palsy
Anupam Singh, Chirag Bahuguna, Ritu Nagpal, Barun Kumar1
Department of Ophthalmology, AIIMS, Rishikesh, 1Department of Medicine (Cardiology), Shri Guru Ram Rai Institute of Medical and Health
Sciences, Dehradun, Uttarakhand, India
Third nerve paralysis has been known to be
associated with a wide spectrum of presentation
and other associated factors such as the presence of
ptosis, pupillary involvement, amblyopia, aberrant
regeneration, poor bells phenomenon, superior
oblique (SO) overaction, and lateral rectus (LR)
contracture. Correction of strabismus due to third
nerve palsy can be complex as four out of the six
extraocular muscles are involved and therefore should
be approached differently. Third nerve palsy can be
congenital or acquired. The common causes of isolated
third nerve palsy in children are congenital (43%),
trauma (20%), inflammation (13%), aneurysm (7%),
and ophthalmoplegic migraine. Whereas, in adult
population, common etiologies are vasculopathic
Introduction
Clinical management of third nerve palsy is most challenging
among all three ocular motor nerve palsies as four out of six
extraocular muscles are involved and therefore must be approached
in a different way. Other associated factors such as the presence of
ptosis, pupillary involvement, amblyopia, aberrant regeneration,
poor bells phenomenon, superior oblique (SO) over action, and
lateral rectus (LR) contracture may further complicate the matter.
Third nerve palsy can be isolated or can occur in association
with other ocular nerve palsies. Isolated third nerve palsy may be
unilateral or bilateral, complete or partial, pupil involving or pupil
sparing, and congenital or acquired.
Correspondence:
Dr. Anupam Singh, Department of Ophthalmology, AIIMS,
Rishikesh 249 203, Uttarakhand, India.
Email: dr.anupamsingh@gmail.com
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DOI:
10.4103/0974-620X.184509
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disorders (diabetes mellitus, hypertension), aneurysm,
and trauma. Treatment can be both nonsurgical and
surgical. As nonsurgical modalities are not of much
help, surgery remains the mainstay of treatment.
Surgical strategies are different for complete and partial
third nerve palsy. Surgery for complete third nerve palsy
may involve supramaximal recession resection of
the recti. This may be combined with SO transposition
and augmented by surgery on the other eye. For partial
third nerve, palsy surgery is determined according
to nature and extent of involvement of extraocular
muscles.
Keywords: Superior oblique transposition, surgical
management, third nerve palsy
The common causes of isolated third nerve palsy in children are
congenital (43%), trauma (20%), inflammation (13%), aneurysm
(7%), and ophthalmoplegic migraine. Whereas, in the adult
population, common etiologies are vasculopathic disorders
(diabetes mellitus, hypertension), aneurysm, and trauma.
Treatment can be both nonsurgical and surgical. As nonsurgical
modalities are not of much help, surgery remains the mainstay of
treatment. Surgical strategies are different for complete and partial
third nerve palsy.
Etiopathogenesis
Several studies have reviewed oculomotor, trochlear, and
abducens cranial nerve palsies in the overall population. The
largest of these was from the Mayo[1] clinic: 4000 cases of cranial
nerve palsies were reviewed. According to this study, third nerve
palsy contributed to 28% of the total cases of ocular nerve palsies.
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Cite this article as: Singh A, Bahuguna C, Nagpal R, Kumar B. Surgical
management of third nerve palsy. Oman J Ophthalmol 2016;9:80-6.
2016 Oman Ophthalmic Society|Published by Wolters KluwerMedknow
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Singh, et al.: Third nerve palsy management
Sixth nerve palsy was the most common (43%), and fourth cranial
nerve palsy (15%) was the least common.
Berlit[2] evaluated 412 patients with isolated and acquired ocular
nerve palsies attending the acute centers of neurology Heidelberg
and Mannheim between 1970 and 1984 in a retrospective study.
Oculomotor nerve palsies were more frequent (41.7%) than the
abducens (40%), the trochlear nerve (6.1%) or combined ocular
motor nerve palsies (12.1%).
Paresis of oculomotor nerve showed no pupil involvement in
62.7% of patients; this applied in particular to III nerve palsies
of vascular (69%), inflammatory (68%), and undetermined
origin (71%). In 92% of patients with tumor and in 78.5% with
aneurysm the pupil was fixed and dilated on examination. The
result of this study was in contrast to other series which report
sixth nerve palsy as the most common ocular motor nerve palsy
followed by third and fourth nerve palsies.[35]
Rucker[6] in 1958 presented a comprehensive review of causes
of paralysis of ocular motor nerve palsies. He included 1000
cases of cranial nerve palsies. Isolated third nerve palsy was
present in 34% of the cases preceded by sixth nerve palsy in
41% of cases. In 28% of the cases of third nerve palsy, no cause
could be determined. In rest of the cases, common causes were
aneurysms (19%), vascular disease (18%), head trauma (15%),
and neoplasm (10%). Rucker[7] again in 1966 undertook a study
for another 1000 cases to determine the relative frequency of the
various etiologies.
Richards et al.,[8] in 1992, reviewed 1278 cases of cranial nerve
palsies. They included both congenital and acquired cases. The
sixth nerve palsy was the most commonly affected nerve followed
by the third and fourth cranial nerve palsies, respectively. For
isolated third nerve palsy, vascular, and undetermined causes were
the most common. Aneurysms were seen less commonly as the
cause.
Green et al.,[1] in 1964, reviewed 130 patients of acquired third
nerve palsy. Their study revealed that the incidence of isolated
ocular nerve palsy is low in the first decade and increases each
decade up to the seventh decade and then decreases precipitously.
About 75% of the patients were over the age of 40 years.
Vascular aneurysms were the most common cause in their series
accounting for 29.2% of the total cases. Diabetes (19.2%), neuritis
(15.4%), trauma (10.8%), tumors (3.8%), syphilis (9.2%), and
miscellaneous (3.8%) were among other etiologies.
Harley,[9] in 1980, reviewed 121 pediatric patients with third,
fourth, sixth, and multiple nerve palsies. Third nerve palsy
accounted for 26% of all the cases. Among 42 cases of third
nerve palsy, 15 were congenital, 4 were posttraumatic, 3 were
postinflammatory, and 5 were with vascular etiology.
Thirty cases of isolated third nerve palsy under the age of 20 years
were studied at John Hopkins Hospital over a period of 25 years
Oman Journal of Ophthalmology, Vol. 9, No. 2, 2016
by Miller.[10] Nearly 43% of the cases were of congenital etiology.
Acquired were most commonly due to trauma and infection
followed by neoplasms, aneurysms, and ophthalmoplegic
migraine.
Tiffin et al.[11] performed a retrospective study of all patients with
acquired III, IV or VI cranial nerve palsy who were seen in the
orthoptic department at Ninewells Hospital, Dundee, over 9year
period from 1984 to 1992. A total of 165 cases were identified.
VI nerve palsies accounted for the majority of the patients (57%),
with IV nerve palsies (21%) occurring more frequently than III
nerve palsies (17%) and multiple palsies (5%). About 35% of cases
were of unknown etiology and 32% of vascular etiology. About
57% of all patients made total recovery (in a median period of
3 months) and 80% made at least a partial recovery. The results
are contrasted with those of previous studies.
Victor[12] studied 16 children with congenital unilateral
oculomotor nerve palsy at John Hopkins Hospital. Ing et al.[13]
reviewed 54 children with the third nerve palsy. In their series,
20% of the cases were congenital. Acquired cases were most
commonly due to trauma (57%) followed by inflammation (13%).
Ng and Lyons,[14] in 2005, studied 18 children under 14 years of
age with oculomotor nerve palsy; of which, 10 were male and
8 were female. Thirteen of the 18 (72%) children were within an
amblyogenic age group, defined as 8 years or less. The etiologic
mechanisms were congenital in 6 patients (33%), traumatic
in 5 (28%), neoplastic in 4 (22%), vascular in 2 (11%), and
migrainous or parainfectious in 1 (6%).
The most common mechanism of isolated, congenital third nerve
palsy is a perinatal injury to the peripheral nerve. Nuclear lesions
are not presumed to be cause in these cases.[12,15] Congenital cases
show predominance for the right eye.[10,12,13]
This is assumed to be related to birth trauma as left
occipitotransverse position of the fetus is the most common
position of occiput during labor.[13] Most of the congenital cases
were thought to be isolated without any associated abnormalities;
however, some reports have been made about the associations
of congenital oculomotor nerve palsies. Balkan and Hoyt,[15]
in 1984, have described few patients of congenital third nerve
palsies with associated neurological deficits consisting of
contralateral hemiplegia in 3 patients, monoplegia in 1 patient,
generalized developmental delay in 2 patients. Keith,[16] in 1987,
reported 1 patient with developmental delay and autism, 1 with
spina bifia, 1 with Goldenhars syndrome and 1 patient with
enlarged ventricles and temporal lobe hypoplasia. Hamed,[17] in
1991, described 2 patients of congenital third nerve palsy with
hemiparesis, 2 with hydrocephalus, 1 with spastic paraparesis,
1 with facial paresis, 1 with septooptic dysplasia, 1 with optic
tract syndrome, 1 with small R midbrain and paresis of cranial
nerves VIIXII and 1 patient with Goldenhars syndrome and
hydrocephalus. After these case reports, Ing et al.,[13] in 1992,
described 2 cases of congenital oculomotor nerve palsy with
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Singh, et al.: Third nerve palsy management
cerebral palsy and 1 with Mobius syndrome. In 1997, Tsaloumas
and Willshaw[18] reported developmental delay, seizures, and
behavioral problems in 3 patients of congenital third nerve
palsy; cerebral palsy in 1 patient, brainstem infarct in 1 patient,
cerebellar infarct in 1 patient, Chiaris malformation in 1 patient,
midline midbrain lesion in 1 patient, and intraconal hemangioma
in 1 patient. White et al.[19] have reported two cases of congenital
third nerve palsy with facial hemangioma, cerebellar hemangioma,
and apparent gaze palsy. Two cases of congenital oculomotor
nerve palsy with neurological deficits and central nervous system
(CNS) abnormalities were reported by Sun and Kao.[20] One of
these patients had hypoplasia of midbrain and corpus collosum
and another one had ventricular dilatation and absence of septum
pellucidum (de Morsiers syndrome).
In 1999, Mudgil and Repka[21] reported cerebrovascular accident
in 4 patients, arteriovenous malformation in 1 patient, posterior
fossa arachnoid cyst in 1, Mobius in 1, craniocynostosis in 1,
brainstem atrophy in 1, and ventriculomegaly in 1 patient.
Recently, Ng and Lyons,[14] in 2005, described panhypopituitarism
along with optic nerve hypoplasia, sensoryneural hearing loss,
choroids plexus cyst in 1 patient of congenital oculomotor nerve
palsy, and holoprosencephaly with CNS migration defect in 1
patient.
The incidence of amblyopia of affected eye is higher in congenital
cases of third nerve palsy.[13] In Victors study, 9 out of the 12 cases
had amblyopia.[12] The best visual acuity in these amblyopic eye
was 6/12. In a study by Ing et al., 5 of 11 cases of congenital
palsy had vision of 6/12 or better.[13] Sometimes, nonpalsied
eye may develop amblyopia instead of palsied eye. It could be
possible either due to the fixation preference of the affected eye
or coexisting nystagmus which gets dampened in more paretic
eye.[22]
Pupil is in the majority of cases of third nerve palsy.[17] The
involved pupil can be either fixed and dilated due to the loss of
innervations to the papillary sphincter or miotic due to aberrant
innervation.
Third nerve palsy is sometimes complicated due to aberrant
innervation. This is seen in both acquired and congenital
cases.[10,13] Miller documented aberrant regeneration in 8 out of
13 congenital cases, whereas Victor[12] in 10 out of 16 cases. In case
acquired third nerve palsy, etiology varies in different age groups.
In children, trauma (20%), inflammation (13%), tumors (10%)
are the most common causes, whereas in adults, vasculopathic
etiologies, aneurysms, and trauma are the main etiologies.
Traumatic nerve palsies are more common in young adult males.
In one study by Elston males accounted 16 out of 20 cases were
males.[23] Third nerve is usually involved in severe, highspeed
closed head injury by either avulsion from the mesencephalon,
primary contusion necrosis or intra and perineural hemorrhage
in the subarachnoid space.[24]
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The third nerve can be involved at any level right from the
level of its nucleus in the midbrain to its area of supply in the
orbit.[25] Nuclear lesions are commonly due to vascular pathology,
demyelination or neoplasms. These lesions have variable
presentation depending on the involvement of various subnuclei.
Nuclear lesions usually present as unilateral third nerve palsy
with contralateral involvement of superior rectus (SR) and
bilateral ptosis, or bilateral third nerve, with or without internal
ophthalmoplegia.
Fascicular lesions like nuclear ones are also because of vascular
pathology, demyelination or neoplasms.[25] These lesions may
involve the surrounding brainstem structures and thus can
present with signs of contralateral hemiplegia or contralateral
intention tremor and ataxia.
Peripheral nerve involvement is relatively more common. The
interpeduncular part can be involved by aneurysm, trauma, or
meningitis. Isolated superior[26] or inferior division[27] palsy
is relatively less common. Superior division involvement has
been reported due to lesions in the anterior cavernous sinus.[28]
Isolated inferior division palsy has been reported with local orbital
disease or trauma, viral, ophthalmoplegic migraine, vasculitis,
demyelinating disease, or unknown pathology.[29]
Third nerve involvement due to cavernous sinus pathology
usually present with multiple nerve palsy. Orbital pathology may
be in the form of pseudotumor, tolosa hunt syndrome, traumatic
neuropathy, and tumor involvement. These patients usually have
other localizing signs such as pain, paresthesias, proptosis, and
compressive optic neuropathy.
Management
The management of patients with oculomotor nerve palsy is one of
the most challenging issues for the strabismus surgeon. Each patient
has different presentation depending on the extent of the paresis,
recovery and presence of aberrant regeneration or other associated
factors. Therefore, management of every patient varies accordingly.
In children, presence of amblyopia and loss of binocularity, due
to the large angle of incomitant strabismus and associated ptosis
further complicate the management of third nerve palsy.
Nonsurgical Management
The goal of management can be short and longterm.
Nonsurgical options are usually indicated as shortterm measures
in the acute phase of acquired palsy, which may last as long as 6
months. It is also indicated as an alternative to surgery when it is
contraindicated.
Occlusion of one eye with a patch, opaque contact lens or blurred
spectacle lens is helpful in case of distressing diplopia. In cases
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Singh, et al.: Third nerve palsy management
with levator palpebrae involvement, the ptosis itself acts as a
natural patch for relieving diplopia.
Prisms can be of use in certain cases where surgery is
contraindicated and in cases with partial paralysis of the third
nerve with the residual function of medial rectus (MR). However,
even in these cases, prism therapy has a limited role as aligning
the visual axes with prisms can be difficult in view of multiplanar
nature of diplopia.
Use of botulinum toxin is another nonsurgical option in the acute
phase of partial third nerve paresis. This is, especially useful in
cases of isolated involvement of MR muscle.
It paralyses the antagonist LR temporarily and thus neutralizes
horizontal deviation in the primary position. It also prevents
contracture of LR muscle. After recovery of the injected muscle,
the remaining vertical deviation may need to be corrected by
prisms or surgical therapy. Some patients may not need surgery
later on. Use of botulinum toxin for vertical muscle imbalance is
rarely indicated due to the high rate of complications associated
with this. SR should not be injected as ptosis can occur if toxin is
placed into the levator SR complex. Injection of inferior rectus
(IR) may be done in cases of isolated SR weakness.
For children who are susceptible to amblyopia, appropriate
refractive error correction and occlusion therapy with a close
followup is advised. This should be followed by early surgery
after any progressive condition is ruled out.
Surgical Treatment
Surgical treatment depends on type (complete/incomplete) and
severity of the paralysis and presence of other associated factors.
Although various surgical options are there, success of these is
hampered by the presence of associated factors such as pupillary
involvement, ptosis, poor bells phenomenon, and aberrant
regeneration. Surgical treatment is advised after a period of 6
months in acquired palsies.
Complete Third Nerve Palsy
In complete palsy, goal of surgery is primary position alignment,
compromising the ocular motility of the involved eye.
Surgery Only on the Affected Eye
Helveston[30] has described supramaximal recessions of LR
(1416 mm) and large resection of MR (814 mm) for correcting
the horizontal deviation in primary position.
Kattleman et al.[31] have also advised supramaximal medial and
LR surgery for the correction of horizontal deviation in primary
position. Large resection of a completely paretic muscle, however,
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accomplishes little. The eye may become exotropic again with
time as the LR muscle undergoes chronic contracture and the
resected muscle elongates.[32,33]
Knapp[34] described a method of fixing the eye in the primary
position with a Callahan suture after recessing all of the temporal
tissue to the lateral rim of the orbital bone.
Kse et al.[33] advised achieving primary position alignment in
patients of total third nerve palsy using surgery on the horizontal
and IR muscles in one session.
According to them it is a safe, simple, and effective procedure and
can be regarded as a firstchoice operation in total oculomotor
nerve palsy.
Villaseor Solares et al.[35] advised ocular fixation to the nasal
periosteum with SO tendon to achieve longterm primary
position alignment in complete oculomotor paralysis. A maximal
recession of LR muscle is done concurrently to weaken and
correct contracture of the LR. This procedure is technically quite
challenging.
Partial Third Nerve Palsy
In partial third nerve, the goals of surgery are, good primary
position alignment, to create, center and enlarge the field of
binocular single vision along with improving motility in certain
cases, alleviation of abnormal head posture as well as the
elimination of diplopia.
Surgical options vary depending on muscle involved, the amount
of recovery and contracture of the direct antagonist of the
paralyzed muscle.[25,29]
MR resection along with antagonist LR recession can be done in
cases of isolated MR involvement. Similarly, for isolated vertical
muscle involvement, the paretic muscle with residual function is
resected and the antagonist is recessed.
If the operated eye still remains hypertrophic, downward
transposition of the horizontal muscles can be done. If the SO
tendon has already been transposed to the SR muscle, the SO
tendon can be remobilized and inserted on the superior aspect of
MR muscle (Peter and Jackson transposition).[36,37]
In cases of paresis of superior division of the third nerve where
elevation is affected, transposition of medial and LR (Knapps
procedure) can be done near the insertion of SR if forced duction
test (FDT) is negative for IR.
In case FDT is positive for IR, IR recession (56 mm) is
recommended. All the lower lid retractors should be separated
from the muscle properly to avoid postoperative lid changes.
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Singh, et al.: Third nerve palsy management
In cases of palsy of inferior division of third nerve, Kushner[38]
described horizontal muscle recession and resection combined
with inferior transposition which was disappointing.
Knapp, in 1978,[39] suggested transposition of the LR muscle to
the site of insertion of the IR and transposition of the SR to the MR
area, combined with tenotomy of the SO muscle to align the eyes in
primary position. Kushner also achieved satisfactory results with
this procedure in five patients. Although transposition of a muscle
does not actually create an effective duction in the direction in
which the muscle is transposed, it does provide some active force
in that direction. This is supposed to stabilize the eye and guard
against a drift toward undercorrection. Weakening of SO corrects
the abnormal intorsion due to unopposed action of SO muscle.
If there is no MR function but meaningful residual SR and IR
function, both vertical rectus muscle may undergo a small resection
(to enhance the transposition medially) and be transposed to the
MR insertion.[26] In all situations, it is advised to measure torsion
adequately and treat it appropriately.
In selective IR palsy, horizontal recti can be transposed inferiorly
in relation to the IR.[40]
Surgery on Superior Oblique
Superior oblique transposition
If MR lacks any function due to complete palsy; other surgical
options are required to improve adduction. In these cases,
transposition of SO tendon is usually necessary to exert a tonic
adducting force to the globe. The procedure was described initially
by Peter in 1934[36] followed by Jackson in 1952.[37]
In this procedure, the trochlea is fractured; the SO tendon is
removed, advanced and attached to sclera near the insertion of
MR muscle. By placing the tendon in this position, the secondary
abducting and depressing actions of the SO muscle are eliminated
and changed to adduction which counters residual LR function.
Similar procedure was utilized by Reinecke[41] in 8 cases,
Helveston[42] in 1 case and Metz and Yee[43] in 1 case.
However, they felt that this procedure is technically difficult; the
SO tendon can be severed inadvertently at trochlea, especially in
adult patients with calcified trochlea. Consecutive hypertropia
and orbital hemorrhage were also seen in some patients.
To avoid these difficulties, Scott, in 1977,[44] described an
alternative technique of transposition of SO tendon without
tracheotomy. In this procedure, SO muscle is first tenotomised at
the medial border of SR muscle. The tendon is sutured to the sclera
2.03.0 mm anterior to the medial side of the SR muscle insertion.
Using this technique, Scott achieved a good result in a patient of
congenital third nerve palsy. Though this procedure is technically
less difficult, carry fewer risks of surgical complications and has
the advantage of reversibility, initial reports with this procedure
were not satisfactory. Harley[45] observed that less adduction is
84
achieved by this procedure than with procedures of Peter and
Jackson. Saunders and Rogers[46] also obtained unsatisfactory
results in four eyes of three patients with oculomotor nerve
palsy with Scotts procedure. Postoperatively, they reported
inadequate horizontal alignment, hypertropias, and paradoxical
eye movements.
In contrast, Maruo et al., in 1996,[47] obtained satisfactory results by
transposing the SO tendon without trochleotomy in combination
with the recession of lateral and superior recti muscles. They
achieved excellent or good results (excellent defined as pressure
prism diopter [PPD] 4 and good as PPD 7) in 82% of patients
of incomplete third nerve palsy. However, the rate for complete
paralysis was low at 61%. They concluded that SO transposition by
Scotts method was effective procedure in achieving a satisfactory
and stable primary position alignment in complete third nerve
palsy. They further concluded that there was no added benefit of
adding MR resection when performing SO transposition, although
combination with the recession of the LR muscle greatly improved
the effectiveness of the procedure. To combat any induced vertical
deviation with SO transposition they combined recession of SR in
cases with no vertical deviation in primary position. Cases with
primary position hypotropia did not require SR recession.
Their results were also supported by Gottlob et al.[48] He treated
seven patients with unilateral third nerve palsy without MR
muscle function, by Scotts procedure in combination with large
LR recession. All patients were followed between 1 and 8 years.
Four patients were orthotropic in the primary position which was
maintained with one operation. One patient had small residual
exotropia. Two patients needed two additional procedures and
were subsequently orthophoric in primary position. In most
of these patients, they did about 14 mm of LR recession. Their
results were comparable with those who underwent the procedure
of Peter and Jackson.
There are opposing opinions as to the effectiveness of performing
the transposition of the SO muscle as well.
Fink[49] believes that the function of the SO muscle is lessened.
Jampolsky[50] found the method effective only when the palsied
eye was used as the fixing eye. Postoperative complications such
as hypertropia, limitation of infraduction, and V pattern deviation
has been reported.[47] In 2 of 8 cases reported by Reinecke,[41]
hypertropia existed; even though, the horizontal deviation was
corrected.
Superior oblique tenotomy
Because of overacting SO muscle in third nerve palsy marked
exotropia in downgaze can lead to an unsightly A pattern and
incyclotorsion. SO weakening surgery (SO tenotomy) can be a
good option for these cases. As the superior and inferior recti
are usually involved to the same degree so, the vertical position
is only slightly influenced by the depressor effect of the SO in
the abducted position.[25] Biglan[51] performed SO tenotomy in
1 patient of postmeningitis oculomotor nerve palsy and reported
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good horizontal alignment but postoperative hypertropia of 4 PD.
The fundus incyclotorsion was also corrected.
Surgery on the Other Eye
Surgery is usually performed on the affected eye first. If the
deviation is sufficiently large; however, horizontal muscle surgery
may be necessary on the fellow eye.
Gottlob et al.[48] proposed that this is, especially beneficial in cases
with signs of aberrant regeneration (e.g., lid opening in adducted
position). The procedure of the horizontal recti in the unaffected
eye is an effort to raise the affected blepharoptosis eyelid. In these
cases, not only primary position alignment but also lid position
was better after operating on horizontal recti of the fellow eye. The
noninvolved eye of these patients was moved toward an adducted
position and abducting impulses were, therefore, needed to gaze
straight ahead. According to Herings law, this stimulated nerve
fibers to the medial recti muscles of the paralytic muscles that
were subsequently innervating the levator palpebrae superioris
muscle.
Main advantages proposed of this new approach were the need
of a single surgery rather than multiple procedures, which
reduces patients discomfort, inconvenience and expense, and
avoidance of complications of a conventional ptosis surgery
(ectropion, entropion, and lid margin peaking). Noonan and
OConnor[52] later on utilized this concept of fixation duress in
1995 to correct vertical deviation and pseudoptosis in patients
of third nerve palsy. They proposed that by decreasing the ability
of the noninvolved eye to elevate, fixation duress was created
which eliminated the secondary deviation that characteristically
occurs in such patients when the involved eye fixates. As a
result of this technique, both eyes in all patients on attempted
fixation are under similar duress, therefore requiring equal
amounts of stimulation to move into the primary position.
When the fixation duress is sufficient, elimination of the
hypotropia and pseudoptosis is achieved. The exotropia was
corrected by a combination of the MR resection, LR recession
of the paretic eye and an LR recession in the fellow eye. The
amount of horizontal recti recession/resection was depending
on the deviation measured with fixing eye. They also weakened
the SR of the normal eye to limit the elevation of that eye. In
certain cases where needed, IR of the noninvolved eye was also
resected. Only one patient had a residual exotropia of 20 PD.
They achieved cosmetically satisfactory results in other two
patients with this procedure.
Sato et al.[53] recommended myectomy of LR muscle to accomplish
a supermaximal weakening effect of abduction in patients with
complete third nerve palsy. Postoperatively, his patient still had an
exotropia of 45 PD. Then, in the second sitting, he did resection
of the MR and recession of LR of the nonaffected eye. Primary
position alignment in his case was then achieved without any
noticeable limitation of abduction in his cases.
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Surgery Only on the Nonaffected Eye
Surgical techniques involving the normal eye were also
recommended by Parulekar and Elston.[54] They described a
surgical plan to simultaneously correct the ocular misalignment
and the pseudoptosis resulting because of aberrant regeneration.
They did large recession of the LR (78 mm) and a smaller
MR resection on the nonparetic eye of four cases to correct the
horizontal misalignment, the amount of surgery being based on
the ocular deviation measured with the dominant eye fixing. To
this, they combined downwards transposition of the insertions
of the medial and lateral recti to correct the vertical deviation.
No surgery was performed on the lids of the paretic eye. They
used this technique successfully in four cases of third nerve palsy
with aberrant regeneration (three traumatic and one congenital).
This technique involved setting the nonparetic eye in a position
of relative adduction. To maintain the eyes in the primary
position, increased innervation of the LR of the nonparetic
eye is needed and the paretic eye adducts. As a result of the
misdirectionregeneration, the levator is stimulated and the ptotic
lid is elevated in the primary position. Because near maximum
innervation is flowing to the MR (so as a result to the levator)
to maintain the eyes in the primary position, there is minimal
further stimulation of the levator in attempted downgaze, and the
pseudoVon Grafes sign is minimized.
Fellow eye muscle surgery is also described in certain cases of
partially recovered third nerve having no diplopia/deviation in the
primary position, but complaining of diplopia in the gaze of the
affected muscle. In such cases, fade operation of the other eye
synergist muscle is advised to provide comitance and to relieve
diplopia in the affected gaze.
Conclusion
Although abovementioned studies have reported satisfactory
outcomes in a number of patients of the third nerve palsy with
various surgical techniques, satisfactory ocular alignment still
remains a challenge for an ophthalmologist in third nerve palsy.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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Oman Journal of Ophthalmology, Vol. 9, No. 2, 2016