A hypertropia is a form of vertical strabismus where one eye is deviated upwards in comparison to the fellow eye. The term of hypertropia is relative to the fellow eye which, by analogy is the hypotrpoic eye- meaning that is deviated downwards. Depending on which eye is fixing, a hypertropia of one eye is the same entity as a hypotropia of the fellow eye, according to Hering’s law. By convention, the designation of the vertical strabismus is made according to the hypertropic eye. If it behaves the same in all fields of gaze or differently in different fields of gaze, it is classified as comitant or incomitant, respectively.
Due to restrictive processes of the elevators of the involved eyes vs depressors of the fellow eye or due to paretic or pseudo-paretic processes of the depressors of the involved eye vs elevators of the fellow eye
Due to a tight muscle
Is one of the most common cause of vertical strabismus. Hypotropia is due to a restrictive inferior rectus muscle
Other features: Compensatory face turn and chin elevation away from the affected side.
Although any extra-ocular muscle can be involved, the IR is the most frequently affected, followed by the medial rectus . Intraocular pressure may increase when looking away from the restriction  Other clinical signs are proptosis; lid retraction; compressive optic nerve dysfunction; conjunctival hyperemia and chemosis and corneal affections due to exposure
Vertical deviation, due to restrictive limitation of elevation, especially in adduction - Y-pattern.
Other features: Face turn to the contralateral side; compensatory chin elevation.
- Congenital (Ex.: Inelasticity of the SO muscle-tendon complex; pseudo-Brown's syndrome due to inferior orbital adhesions; inferior displacement of the lateral rectus). A spontaneous resolution of congenital Brown’s syndrome has been reported.
- Iatrogenic (Ex.: Following glaucoma, oculoplastics or strabismus surgery; ENT surgery)
- Inflammation of the trochlea (Ex.: Rheumatoid arthritis; systemic lupus erythematosus)
- Nasal sinus infection
- Tight superior oblique muscle (Ex.: Thyroid ophthalmopathy; secondary to superior oblique overaction)
- Hurler-Scheie syndrome
Inferior Oblique Overaction
Ipsilateral hypertropia that increases on adduction to the contralateral side. Ex.: Left inferior oblique overaction causes a left hypertropia in right gaze.
Other features: If primary and bilateral, it gives rise to a Y-pattern, with divergence in upgaze; if secondary, i.e. due to a paresis of another vertical muscle, it may give rise to a V pattern, with additional convergence in downgaze. When it is primary (not related to a paresis of another vertical muscle), the head tilt- test is negative (the superior rectus and oblique muscles are ‘’working’’).
It is frequently bilateral and associated with a horizontal strabismus, although it may be isolated.
- Secondary to an ipsilateral superior oblique paresis or a contralateral superior rectus paresis.
Superior Oblique Overaction
Vertical deviation, that increases on adduction to the contralateral side. Ex.: A left superior oblique overaction causes a right hypertropia on right gaze.
Other features: Intorsion and abduction in downgaze. If congenital, the intorsion is frequently only objective and not subjective, since there is sensory adaptation. It frequently coexists with an underaction of the contralateral IR and intermittent exotropia. Sometimes it can give rise to an acquired Brown’s syndrome, due to SO contracture (for the differential diagnosis between SO overaction and Brown’s syndrome, see the differential diagnosis section). A vertical deviation in primary position is more frequently associated with a unilateral or asymmetric SO paresis. When bilateral, it frequently gives rise to lambda-pattern, with accentuated exotropia in downgaze.
It is more frequently bilateral. It often coexists with an intermittent exotropia or other forms of horizontal strabismus.
- Secondary to a contralateral inferior rectus paresis.
Due to a weak muscle
Unilateral Superior Oblique Paresis
Hypertropia that increases on adduction to the contralateral side and head tilt to the side of the affected muscle. Ex.: Left superior oblique paresis causes a left hypertropia on right gaze and head tilt to the left.
Other features: Mild extorsion (<10º); compensatory head tilt to the contralateral side and face turn towards the contralateral shoulder, sometimes associated with a facial asymmetry; contralateral inferior rectus overaction (“fallen eye’’); large vertical fusional amplitudes when congenital.
- Congenital and traumatic causes are the most frequent (Congenital causes are frequently due to absent trochlear nerves, muscle hypoplasias or tendon laxity but muscle/tendon agenesis has also been described. Symptoms sometimes arise in late childhood or middle age. If traumatic, it is bilateral until proven otherwise.)
- Neurologic (ex.: Myasthenia gravis)
- Iatrogenic (ex.: Slipped muscle; following tenotomy or tenectomy procedures)
- Diabetic mononeuropathy
- Viral (ex.: Herpes zoster)
- Nasal sinus affections (ex.: Mucocele)
Bilateral Superior Oblique Paresis
Left hypertropia in right gaze, right hypertropia in left gaze, the hypertropia is less evident than in unilateral superior oblique paresis.
Other features: Larger extorsion than in unilateral paresis (>10º); esotropia increasing in down gaze (>10º) – V pattern of the ''arrow subtype''. Sometimes bilateral involvement can be masked due to an asymmetrical involvement. Some signs that can be suggestive of bilateral involvement are the reversal of hypertropia on ipsilateral side gaze and contralateral head tilt, objective fundus extorsion  and a slight IO oblique overaction of the other eye,as sometimes it becomes evident only after a surgical correction.
- Trauma (The IV cranial nerves exit the midbrain very closely so that strong head traumas, or sometimes even small ones, frequently origin bilateral rather than unilateral palsies)
- Congenital (uncommon)
Superior Rectus Underaction of the fellow eye
- Iatrogenic (ex.: Following superior rectus weakening procedures, glaucoma surgery, oculoplastic surgery, scleral buckle insertion.)
- Innervational anomaly of the superior division of the III cranial nerve
- Muscle aplasia
- Neoplastic (ex.: Pineocytoma, orbital tumor)
Monocular Elevation Deficit Syndrome (MEDS)
Limitation of elevation with contralateral hypertropia, previously called double elevator palsy.
Cause: It can have various causes, such as orbital restrictive or neurological causes (supranuclear, nuclear or inflanuclear). Sometimes it can be associated with congenital inferior rectus restriction, superior rectus palsy  or both. 
Inferior Rectus Underaction of the affected eye
Similar to the above Superior rectus underaction
- Iatrogenic (ex.: Overcorrections following inferior rectus weakening procedures as in thyroid ophthalmopathy )
- Innervational anomaly of the inferior division of the III cranial nerve
- Muscle aplasia (The inferior rectus is most frequently affected, it can be associated with craniofacial disorders)
- Neurological (ex.: Myasthenia gravis)
Unilateral Inferior Oblique Paresis
Contralateral hypertropia due to overaction of the yoke muscle (SR). The increase of vertical deviation in adduction and upgaze to the contralateral side. Hypertropia, that increases on head tilt to the contralateral side. Ex.: Left inferior oblique paresis causes a right hypertropia on right and up gaze and head tilt to the right.
It is a rare etiology and a bilateral involvement is very uncommon.
- Most frequently idiopathic or iatrogenic (following anterior transposition surgery – anti-elevation syndrome).
A very rare form of isolated IR affection has been described
Other complex forms of strabismus or involving multiple muscles
Canine Tooth Syndrome
In addition to the restrictive elevation, there is also a SO paresis. It is frequently traumatic.
Pseudoinferior Rectus Palsy
Slight hypertropia in primary position as muscular function is preserved from upgaze to primary position, and a large hypertropia from primary position to downgaze. It can be caused by an adherence of the inferior rectus to the orbital floor following a traumatic fracture, giving rise to a muscle slack in front of the adherence. 
Dissociated Vertical Deviation
Hypertropia of one eye without hypotropia of the fellow eye, that becomes manifest when binocular fusion is interrupted either by occlusion or by spontaneous dissociation.
Other features: Abduction and extorsion. Increased vertical deviation on head tilt to the ipsilateral side.
Most frequently both eyes are affected, although it may be asymmetrical . When bilateral, the vertical deviation of each eye is not related to the other, as in true hypertropia (no yoke muscle overaction is present).
Cause: Any cause leading to a disruption of normal binocular development can be at its origin. Rarely primary.
Displaced Horizontal Recti
If horizontal recti are displaced superior- or inferiorly, they act as additional elevators or depressors. V and A patterns may result simulating oblique muscle paresis/overactions.
- Congenital (ex.: Craniosynostosis; extorted orbit)
- Iatrogenic (ex.: Following strabismus surgery)
- High myopia, where a posterior staphyloma misplaces the lateral rectus inferiorly.
Frequently due to peri-orbital fat adhesions to the eye globe, leading to a restrictive syndrome (Ex.: pseudo-Brown's syndrome), or following retinal surgery:
- Scleral buckle with posterior slippage, entrapment or splitting of extraocular muscles and anterior displacement of an oblique muscle.
- Following ocular surgery (Ex.: Strabismus surgery; glaucoma surgery, especially with the Baerveldt device or due to a mass effect caused by the bubble; oculoplastic surgery)
Sometimes associated with a hypertropia in adduction, due to aberrant innervation of vertical muscles or a restrictive lateral muscle.
Large Angle Exotropia
Hypertropia or hypotropia in in adduction. – X- pattern
Congenital Fibrosis of the Extraocular Muscles:
Ocular Deviation Tests to asses Hypertropia
A light source located in front of the examiner's eyes is directed at the patient's eyes, while the patient is asked to fixate the light source directly. The corneal light reflex is observed. The Hirschberg test is considered normal when the corneal light reflexes are slightly decentered nasally (about 5º, due to angle kappa). In the case of a hypertropia, the light reflex of the deviated eye is located below the light reflex of the fixing eye. The amount of deviation can be grossly estimated by multiplying the mm of deviation by 15PD.
This test uses prisms to complement the Hirschberg test. Prisms are positioned in front of the deviating eye, base-down in the case of a hypertropia, and are progressively increased until a neutral Hirschberg test is obtained. It is particularly helpful in patients that don’t collaborate well in the former test, especially with low visions.
The cover/uncover test allows for the diagnosis of tropias, when performed correctly. In order to achieve this, the physician needs to briefly cover the eye that is fixing and see if there is a refixation movement of the fellow eye. In the case of a hypertropia, the non-fixing eye moves downward as it takes up fixation. If no refixation is observed the other eye may be the fixing one, in which case it is covered and the test is performed again. It is very important for the cover to be very brief, since a prolonged cover will break binocular fusion and provoke a possible phoria that can be misinterpreted as a -tropia. A pure -phoria won’t have a positive cover/uncover test, while a -tropia is also associated with positive alternate cover test.
Simultaneous Prism Cover Test
A test that can be used to estimate the angle of deviation attributable to a -tropia. The amount of PD that have to be added in order to revoke refixation movements in the deviating eye, correspond to the deviation angle. This shouldn’t be confused with the alternating prism cover test for the correction of a -phoria component, in which case binocular fusion is interrupted. In the case of incomitant strabismus due to muscle paresis or restrictive syndromes, one prism is placed over the eye with limited ductions to measure the primary deviation and a second prism is placed in front of the good eye to measure secondary deviation. The deviation is always bigger when the eye with limited ductions is fixing (i.e. the prism is over the normal eye)
Worth 4 Dot Test
Allows for the diagnosis of diplopia and suppression. A different light filter is positioned in front of each eye, a green and a red light filter. The patient is asked to look at 4 different dots: 2 green dots on either side; one red dot on top; one white dot on the bottom, forming a cross. Green dots can only be seen by the eye with the green light filter and the red dot can only be appreciated by the eye with the red filter, while the white dot can be seen by both eyes. If the patient sees 5 lights instead of 4, a diplopia is present. If the lights seen by one eye are below the expected position, it means that eye is hypertropic (the image is projected on the superior retinal quadrants, which perceive the lower visual fields). If the patient sees less than 4 lights, suppression is present.
Red Filter Test
Same principle as the Worth dot test, but with only one light source and one light filter (red) in front of the eye to be examined. The patient seeing a pink light is a normal test result. If two lights are perceived, diplopia is present. If the patient only sees a white light, suppression of the eye with the red filter is present.
Maddox Rod Test
One Maddox rod is positioned in front of each eye, while the patient is asked to look at a light source. This way, each eye will only see one linear streak of light. In order to test for a vertical tropia, the Maddox rods have to be placed in order to create streaks at 180º degrees. If one streak is perceived below the other, a hypertropia/phoria is present. Since the Maddox rod test is highly dissociative, it doesn’t allow for a differential diagnosis between a -phoria and –tropia. Torsion is evaluated by using the Double Maddox Rods.
Bagolini Striated Lens Test
This test is very similar to the Maddox rod test, with the exception that Bagolini striated lenses allow for a better view of the peripheral visual field, giving more binocular clues. This way, less dissociation is present and a better distinction between a small suppression scotoma with peripheral fusion and a large suppression scotoma is possible.
A haploscopic test is a test where different images are presented to each eye, which are independent from one another and can be freely moved. A synoptophore is an example of a haploscopic test. In the case of the synoptophore, the patient is asked to look inside each arm with the corresponding eye, while the arms are freely moveable and present different images to the right and left eye. The subjective angle, is the angle between the two arms, where the patients perceives the images to be fused, i.e. binocular vision is obtained. The objective angle is determined by switching the lights on and off, while changing the angle, until no refixation movements are detectable. It corresponds to the angle obtained through the alternate prism cover test.
Signs and Symptoms
Is not perceived by the patient, but rather by the observer. Suppression happens when the deviation starts in the early years of life (before 6 years of age), when the neuroplasticity of the visual system is still capable of suppressing the image coming from the deviated eye. The amount of suppression, which can vary from small suppression scotomas in binocular fusion to large suppression areas on the affected side and amblyopia, depends on various factors such as the size of the strabismus and age of onset.
For further signs, see diagnosis and physical examination.
Occurs when the deviation is acquired after a significant maturation of the visual system (7 to 8 years of age), when suppressive mechanisms are no longer initiated. Younger children may also have transitory diplopia in acquired forms of strabismus, before suppression kicks in. In the case of a hypertropia, the diplopia is vertical.
Two images are perceived in the same location, due to a misalignment of retinal correspondence points on the fovea. This symptom is rare, when compared to diplopia and the same rules apply for age of patients affected. It has been observed in glaucoma patients with an acquired strabismus (see strabismus following glaucoma surgery), due to tunnel vision and forced use of the fovea.
Differential Diagnosis between a Paresis and a Restriction of the Antagonist
Forced Duction Test: If there is a restriction, forced duction test are positive, while a pure paresis allows full forced ductions.
Saccadic Eye Movements: In the case of a restriction, normal saccadic eye movements can be observed until the full restrictive amplitude is achieved, where it stops abruptly. In the case of a palsy, abnormal saccadic eye movements are present.
Intraocular Pressure: Restrictions may lead to increase IOPs when the eye is moving against the restriction.
Lid fissure: Restrictions may cause lid fissure narrowing, while a paresis causes lid fissure widening.
Bielschowsky Head Tilt Test
Allows differentiating whether a vertical deviation is due to a vertical rectus muscle paresis or an oblique muscle paresis. When the head is tilted, extorsion and intorsion movements are executed. The superior oblique and superior rectus muscles are intortors and the inferior oblique and inferior rectus muscle are extorters. When there is an upshoot on a head tilt, it means that there is an imbalance between vertical forces and that one of the four torsional muscles is not working properly. When there is and upshot on the side of the head tilt, either the ipsilateral SO or the contralateral IO is paretic, when there is an upshot on the contralateral side of the head tilt, either the ipsilateral IR or the contralateral SR is paretic. To distinguish between the two entities, see the parks-three-step-test bellow.
Oblique muscle overactions are associated with a negative head-tilt-test.
Which muscle is the culprit? The Parks-three-step-test allows determining which muscle is at the origin of a vertical deviation, in cases of single muscle paresis. A hypertropia can be caused by 4 different muscles, for example, a right hypertropia can be caused by a paresis of a right eye depressor (right SO, right IR), or a left eye elevator (left IO, left SR). First of all, the primary position of gaze is inspected and it is determined which eye is hypertropic. Second, the physician has to determine to which side of gaze the hypertropia increases, for example, if a right hypertropia increases on left side gaze either the RSO or the LSR is affected. This second step reduces the possibilities to 2 muscles; either an oblique or a rectus muscle is affected. The third and last test allows the examiner to determine if the rectus or the oblique muscle is affected: the bielschowsky head tilt test, already described above.
The tree-step-test is not diagnostic when more than one muscle is affected or there is a restrictive cause; there are some situations where a false positive result can lead to a misdiagnosis: A paresis of more than one vertical muscle, contracture of the vertical recti, previous vertical muscle surgery, skew deviation, myasthenia gravis, dissociated vertical deviation and small vertical deviations associated with horizontal strabismus.
Differential Diagnosis between Brown’s Syndrome, Superior Oblique Overaction and Inferior Oblique Paresis
Patients with Brown’s syndrome will have a positive forced-duction test especially evident on the Guyton’s exaggerated forced-duction test. In Brown’s syndrome there is a Y-pattern, whereas a lambda pattern is present in SO overaction and an A pattern in IO paresis. To distinguish between a IO paresis and a SO overaction see head-tilt-test above. To make everything a bit more confusing, a Y pattern can also be present when there is an aberrant innervation of the lateral recti, in upgaze, or in the case of a bilateral inferior oblique overaction (see above).
Differential Diagnosis between DVD and Inferior Oblique Overaction
In inferior oblique overaction there is an increase of ipsilateral hypertropia in adduction to the contralateral side with a contralateral hypotropia, whereas in DVD, there is a hypertropia in adduction as well as in and abduction without a true contralateral hypotropia, when binocular fusion is interrupted. In order to evaluate this, the physician needs to check for a vertical deviation of the occluded eye, while the patient looks either side. Translucent occluders of Spielman are particularly helpful.
- If vertical deviation in primary position of gaze, attributable to a restriction of the IR on forced ductions: Inferior rectus recession. In the case of a large angle strabismus, a contralateral superior rectus recession may be indicated.
- If superior rectus palsy is: Superior transposition of half tendon lengths of medial and lateral recti or Knapp procedure. In the case of forced duction limitation, add an inferior rectus recession to the former.
- If due to restriction and minimal hypertropia in primary gaze: resection of the ipsilateral IR.
- If a large hypertropia is present on primary gaze position: Ipsilateral IR resection + contralateral SR or IR recessions. An inverse Knapp procedure may be necessary.
- In the case of orbital floor fracture with IR affection:
- Orbital floor repair, if indicated.
- If 8-15PD in primary position: Unilateral IR recession.
- If there is a large hypotropia in upgaze even in the case of a <8PD deviation in primary position: IR recession and an additional contralateral asymmetrical IR recession or contralateral SR recession may be indicated
- If >15PD in primary position: Ipsilateral IR recession plus contralateral SR recession.
- In pseudo-inferior rectus palsy with hypertropia in primary position: Ipsilateral muscle slack reduction through a plication + contralateral IR recession.
Superior Oblique Underaction
- If <10DP hypertropia in primary position, IO overaction more significant than SO underaction (deviation greater in upgaze): Ipsilateral graded inferior oblique anteriorization (weakening procedure)
- If >15DP hypertropia in primary position (or deviation bigger in downgaze): Ipsilateral graded inferior oblique anteriorization + contralateral inferior rectus recession (yoke muscle).
Superior oblique tightening procedures - "tucks"- are indicated in congenital SO palsy with tendon laxity tested through forced duction or when there is minimal IO overaction with the vertical deviation being greatest in downgaze. This procedure may cause iatrogenic Brown syndrome.
- If the deviation has become comitant due to superior and inferior rectus contractures, respective recessions should be performed
In the case of a traumatic cause, it is advised to wait for 6 months and reevaluate for a potential recovery.
- If main problem is extorsional diplopia (as in partially recovered post-traumatic paresis), with minimal hypertropia and V-pattern: Harada-Ito procedure.
- If a big V-pattern, with >15DP esotropia in downgaze and >10º extorsion in primary position is present; reversing hypertropias in sidegaze: Bilateral Harada-Ito + bilateral medial rectus recessions with half-tendon width inferior transpositions or superior oblique tendon tuck + bilateral medial rectus recessions with half-tendon width inferior transpositions.
- If masked bilateral involvement or asymmetric involvement is suspected: Bilateral IO graded anteriorization + contralateral IR recession or bilateral graded IO anteriorization + Harada-Ito procedure on the more affected side.
- If a vertical deviation in primary position, abnormal head posture or diplopia:
- If vertical deviation <10DP: Ipsilateral SO weakening (see superior oblique overaction)
- If vertical deviation of >10DP: Ipsilateral SO weakening + contralateral SR weakening.
Inferior Oblique Overaction 
- If binocular fusion is compromised or for cosmetic reasons: A graded anteriorization of the IO is frequently sufficient. In this procedure it is important to keep the anterior IO fibres posterior to the IR insertion in order to avoid a hypercorrection and consequent hypodeviation.
- If bilateral, even if asymmetric: Bilateral IO weakening procedures (myectomy, recession, anteriorization) should be performed, except if amblyopia is present (surgery on the good eye is discouraged).
- In the presence of a significant Y pattern in upgaze, even if there is no significant deviation in primary position or sidegaze: Bilateral IO weakening procedures
SO weakening procedures: SO expander, tenotomy, tenectomy or recession.
If the patient has binocular fusion, weakening the superior oblique may give rise to extorsional diplopia. In this particular case, horizontal muscle surgery or an expander may be more indicated, as suggested by Wright et al.
In the case of a coexisting DVD, particular care has to be taken since SO weakening procedures may worsen this entity.
- If inflammatory: systemic nonsteroidal antiinflammatory agents, local steroid injection to the trochlea.
- If congenital: There is an indication for surgery if there is a vertical deviation in primary position with an important face turn. SO lengthening procedures are indicated such as: SO expander, tenotomy, tenectomy. With tenotomy and tenectomy, care should be taken for overcorrections.
Duane's Syndrome - the vertical component.
It may be addressed surgically with a Y-splitting procedure of the ipsilateral lateral rectus muscle.
- Relocate horizontal rectus muscle. Hereby, lateral recti are moved towards the open end of the pattern (up in V, down in A), while medial recti are transposed to the closed end of the pattern (down in V, up in A)
It is very important to correctly diagnose the cause of A and V patterns, because one may have the false impression of oblique muscle affection. If the A or V pattern is caused by a horizontal muscle displacement, it responds poorly to oblique muscle surgery.
- Medical: Teprotumumab has recently been approved by the U.S. F.D.A, and may rapidly become the first line therapy . Systemic steroids and external beam radiation may be indicated to control inflammation. 
- Surgical: Strabismus surgery has to be postponed until after orbital decompression procedures have been performed and orbital inflammation is controlled. A waiting period of 6 to 12 month following thyroid function test stabilization is recommended. The procedure of choice is the recession of affected muscles. In the case of IR involvement with a vertical deviation >18-20DP, a bilateral recession is advised. Late overcorrections are frequent. Wright et al. advise the use of non-reabsorbable (ex.:6-0 Mersilene) sutures in order to avoid this complication. The use of adjustable sutures has also been advised by Lueder.
- If cosmetically intolerable wright or if noticeable AA: SR recessions can be performed, although a complete resolution is rarely obtainable.
- If associated with an IO overaction: Sole IO graded anteriorization
- If associated with an SO overaction: Treat the A pattern with horizontal muscle transpositions, or an undercorrected SO weakening procedure, since the latter may aggravate the symptoms of DVD
- If both eyes can fixate: Bilateral SR recessions, with asymmetric recessions if asymmetric
- If overcorrected: Associate an IR plication or resection
- American Academy of Ophthalmology. Strabismus. https://www.aao.org/image/strabismus-5 Accessed January 29, 2020.
- Wright K, Spiegel P, Thompson L. Handbook of Pediatric Strabismus and Amblyopia. Springer, 2006. Print.
- American Academy of Ophthalmol. Pediatric Ophthalmology and Strabismus. BCSC, 2014-2015.
- Prendiville P, Chopra M, Gauderman WJ, Feldon SE. The role of restricted motility in determining outcomes for vertical strabismus surgery in Graves’ ophthalmology. Ophthalmol. 2000;107:545– 549.
- Bartley GB, Gorman CA. Diagnostic Criteria for Graves' Ophthalmopathy. Ophthalmol 1995; 119:792–795.
- Mourits M, Koornneef L, Wiersinga M,Prummel. Clinical criteria for the assessment of disease activity in Graves' ophthalmopathy: a novel approach. Br J Ophthalmol. 1989; 73:639-644
- Mario Salvi, Davide Dazzi, Isabella Pellistri Classification and prediction of the progression of thyroid-associated ophthalmopathy by an artificial neural network. Ophthalmol. 2002; 109:1703–1708
- Ventura MP, Vianna R , Souza J, Solari HP and Curi RLN. Acquired Brown's syndrome secondary to Ahmed valve implant for neovascular glaucoma. Eye. 2005; 19:230–232.
- Prata JA, Minckler DS, Green RL. Pseudo-Brown's syndrome as a complication of glaucoma drainage implant surgery. Ophthalmic Surgery. 1993, 24:608-611
- Neely KA, Ernest JT, Mottier M, Combined Superior Oblique Paresis and Brown's Syndrome After Blepharoplasty. M.Journal of Clinical Neuro-Ophthalmology. 1990, 10:293
- Leibovitch I, Wormald P, Iatrogenic Brown's Syndrome During Endoscopic Sinus Surgery With Powered Instruments. Otolaryngology-- Head and Neck Surgery. 2005, 133:300-301.
- Cooper C, Kirwan JR, McGill NW, Dieppe PA. Brown's syndrome: an unusual ocular complication of rheumatoid arthritis. Ann Rheum Dis 1990;49:188-189
- Alonso-Valdivielso JL, Lario BA, López JA, Tous MJS, Gómez AB. Acquired Brown's syndrome in a patient with systemic lupus erythematosus. Ann Rheum Dis 1993;52:63.
- Thacker NM, Velez FG, Demer JL, Rosenbaum AL. Superior Oblique Muscle Involvement in Thyroid Ophthalmopathy J AAPOS 2005;9:174–178.
- Gregersen E, Rindziunski E. Brown's syndrome. A longitudinal long-term study of spontaneous course. Acta Ophthal. 1993,71:371–376.
- Dawson E, Barry J, Lee J. Spontaneous resolution in patients with congenital Brown syndrome. J AAPOS 2009,13:116–118
- Megha M, Tollefson, Mohney BG, Diehl N, Burke JP. Incidence and Types of Childhood Hypertropia A Population-Based Study.Ophthalmol. 2006;113:1142-1145.
- Mollan SP, Edwards JH,Price A, Abbott J, BurdonA. Etiology and outcomes of adult superior oblique palsies: a modern series Eye. 2009; 23, 640–644
- Gunther K. Superior oblique paralysis. Aust J Ophthalmol 2007;7:44-48
- Yang HK, Kim JH, Hwang JM. Congenital superior oblique palsy and trochlear nerve absence: a clinical and radiological study. Ophthalmol. 2012;119:170- 177.
- Pineles SL, Velez FG, Elliot RL, Rosenbaum AL. Superior oblique muscle paresis and restriction secondary to orbital mucocele. J AAPOS 2007;11:60–61
- Souza-Dias, C. Asymmetrical bilateral paresis of the superior oblique muscle. J AAPOS 2007; 11: 12–16
- Esmail F, Flanders M. Masked bilateral superior oblique palsy. Can J Ophthalmol. 2003;38:476–481.
- Munoz M, Page LK. Acquired double elevator palsy in a child with pineacytoma. Am J Ophthalmol 1994; 118:810-1.
- Farr AK, Guyton DL. Strabismus after retinal detachment surgery Curr Op Ophthalmol. 2000; 11:207-210.
- Munoz M, Parrish Rk. Strabismus Following Implantation of Baerveldt Drainage Devices. Arch Ophthalmol. 1993;111:1096-1099
- Mazow ML, Avilla CW. Restrictive Horizontal Strabismus Following Blepharoplasty. Am J Ophthalmol. 2006; 141:773-774.
- Garg, A, Alio JL. Surgical Techniques in Ophthalmology: Oculoplasty and Reconstructive Surgery. Jitendar P Vij, NDheli, 2010
- Wright KW, Liu GY, Murphree AL. Double elevator palsy, ptosis and jaw-winking. Am Orthopt J 1989; 39:143–150.
- Metz HS. Double elevator palsy. Arch Ophthalmol 1979; 97:901– 909.
- Kim JH, Hwang JM. Congenital monocular elevation deficiency. Ophthalmology 2009; 116:580- 584.
- Pusateri TJ, Sedwick LA, Margo CE. Isolated Inferior Rectus Muscle Palsy From a Solitary Metastasis to the Oculomotor Nucleus. Arch Ophthalmol 1987;105:675-7.
- Spoor TC, Shippman S. Myasthenia Gravis Presenting as an Isolated Inferior Rectus Paresis. Ophthalmol.1979; 86:2158–2160.
- Walker JPS, Congenital absence of inferior rectus and external rectus muscles. Brit. J. Ophthal.1954;38:631.
- Sergott RC, Glaser JS. Graves' ophthalmopathy. A clinical and immunologic review. Surv Ophthalmol. 1981; 26:1-21.
- Brown H. Isolated Inferior Oblique Paralysis: An Analysis of 97 Cases. Trans Am Ophthalmol Soc. 1957;55:415-454
- Castro O, Johnson LD, Mamourian AC. Isolated Inferior Oblique Paresis from Brain-Stem Infarction: Perspective on Oculomotor Fascicular Organization in the Ventral Midbrain Tegmentum Arch Neurol. 1990;47:235-237
- Spoor TC, Shipmann S. Myasthenia Gravis Presenting as an Isolated Inferior Rectus Paresis Ophthalmol. 1979; 86: 2158-2160
- Guyton DL. Dissociated vertical deviation: Etiology, mechanism, and associated phenomena.J AAPOS. 2000,4: 131–144.
- Rosenberg JB, Tepper OM, Medow NB. Strabismus in craniosynostosis.J AAPOS 201350: 140-148.
- Heidary G, Engle EC, Hunter DG. Congenital fibrosis of the extraocular muscles. Ophthalmol. 2008;23(1):3-8.
- Yazdani A, Traboulsi EI. Classification and surgical management of patients with familial and sporadic forms of congenital fibrosis of the extraocular muscles. Ophthamol. 2004;111:1035-1042.
- De Respinis PA, Naidu E, Brodie SE. Calibration of Hirschberg test photographs under clinical conditions. Ophthalmol 1989;96: 944–949.
- Ruttum MS, Shimshak KJ, Chesner M. Photographic measurement of the angle of strabismus. Strabismus and ocular motility disorders. SOMD 1990; 155–160.
- Kushner BJ. Errors in the Three-step Test in the Diagnosis of Vertical Strabismus. Ophthalmol. 1989; 96: 127-132
- Kushner BJ. Pseudo inferior oblique overaction associated with Y and V patterns. Ophthalmol.1991; 98:1500-1505.
- Spielmann A. A translucent occluder for study of eye position under unilateral or bilateral cover test. Am Orthoptics J1986;36:65.
- Plager A, Buckley EG. Strabismus Surgery: Basic and Advanced Strategies. Oxford UP, NY. 2004. Print.
- Romano P, Roholt P. Measured graduated recession of the superior oblique muscle. J AAPOS 1983;20:134–140.
- Berke RN. Tenotomy of the superior oblique for hypertropia. Trans Am Ophthalmol Soc 1946;44:304–342.
- Smith TJ Thyroid-associated Ophthalmopathy: Emergence of Teprotumumab as a Promising Medical Therapy. Best Pract Res Clin Endocrinol Metab. 2020;101383. PMID 32088116
- Cockerham KP, Kennerdell JS. Does radiotherapy have a role in the management of thyroid orbitopathy? Br J Ophthalmol 2002;86:102-107
- Harrad R. Management of strabismus in thyroid eye disease. Eye 2015;29:234-237
- Lueder GT, Scott WE, Kutschke PJ, Keech RV. Long-term Results of Adjustable Suture Surgery for Strabismus Secondary to Thyroid Ophthalmopathy. Ophthalmology. 1992;99:993–997