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Ocular abnormal head posture or torticollis is a frequent sign in pediatric pathology. The incidence is 5,6% in ophthalmological practice and 3,19% in pediatric ophthalmological practice. Causes of ocular abnormal head posture are: incomitant strabismus, nystagmus, refractive errors, palpebral ptosis, neuro-ophthalmological diseases affecting visual field. The abnormal head posture is adopted to improve visual acuity, maintain binocular single vision, center residual visual field with the body or for cosmetic reasons. According to the three main body axes, there are three categories of head orientation: head tilt, face turn, chin-up or down. The most frequent ocular causes of head tilt in children are congenital nystagmus, superior oblique paresis, dissociated vertical deviation, Brown syndrome, refractive errors. Chin-up or chin-down abnormal head postures are most commonly caused by “A” and “V”-pattern strabismus, palpebral ptosis, nystagmus, refractive errors.
Key-words: ocular torticollis, abnormal head posture, head tilt, chin-up, chin-down
Abnormal head position (ahp) or torticollis is frequent in pediatric pathology. One important cause of torticollis is ocular pathology. Ocular torticollis was first described in 1873 by Cuignet . In one series of patients the incidence of ahp is 5,6% in ophthalmological practice . The incidence in pediatric practice is 3,19%. Ocular torticollis is sometimes misdiagnosed because the ocular signs and symptoms are not obvious for the primary care physician or for the experts in other disciplines.
In ophthalmology the preferred terminology is abnormal head posture instead of ocular torticollis but while the patient derives a demonstrable advantage by adopting the head position (improving visual acuity or binocularity) it is more correctly to use the term compensatory head posture (chp).
Etiology and physiology of the abnormal head posture
The sense organs implicated in normal head position are: the retina, the proprioceptors from the neck and the labyrinth with the semicircular canals and utricle. The otolithic apparatus within the utricle responds to static head position and is activated during maneuvers such as head tilting to one shoulder. The semicircular canals respond to dynamic head movements in the three dimensions of space. ibular nuclei in the brainstem and from there rostrally to the vestibular cortex and caudally to the cervical cord and neck muscles. Inputs from cerebellum and neck proprioceptors are also integrated into the system. There are also direct connections between labyrinth and the extraocular muscles activated by the changes in the semicircular canals. Impulses from the retina are responsible for fine adjustments in head position.
Causes of torticollis are:
– Congenital or acquired muscular diseases involving the muscles of the neck (sternocleidomastoid, thoracic and semispinalis being the most important muscles implicated in head and neck posture);
– Congenital or acquired diseases of the spinal column;
– Abnormal neural inputs from the aforementioned sources, including vestibular apparatus.
Ocular torticollis arises from disturbances in the input from the afferent visual pathway, oculomotor nerves or the vestibular apparatus. Congenital or acquired diseases at these levels cause alterations in the normal input transmission to the neck muscles and the torticollis appear.
Causes of ocular chp are:
– Incomitant strabismus which can be innervational (muscle underaction by paralysis or myasthenia, or muscle overaction by excessive innervation) or mechanical (diseases involving muscles, soft tissues or bones of the orbit). The definition of incomitant strabismus is that the deviation is not the same in all positions of gaze (like in concomitant strabismus). There is a position of gaze with maximal eye misalignment (the gaze position in which the effect of the involved muscle is most readily observed). Incomitance may be horizontal (sixth nerve paresis, duane syndromes, orbital fracture, myasthenia, congenital fibrosis syndrome, infantile esotropia), vertical (fourth nerve paresis, “a” or “v”-pattern strabismus, dissociated vertical deviation, monocular elevation deficit, brown syndrome, orbital fracture, myasthenia, congenital fibrosis syndrome) or both;
– Nystagmus as an involuntary, rhythmic toand- fro oscillation of the eyes. Based on the direction of the oscillations it can be torsional, horizontal, vertical or a combination of them. As a general rule, the compensatory head position is adopted according to the type of nystagmus: if torsional, the compensatory head posture is head tilt, if horizontal, face turn and if vertical, the posture will be chin-up or chin-down. Most of the types of nystagmus are associated with null zone. This is a particular position of the eye into the orbit, at which nystagmus is minimal. Chp is generally used to bring the eye in that position which lessen the oscillations and improve visual acuity;
– Refractive errors in one of the three forms: myopia, hypermetropia and astigmatism;
– Permitting foveal fixation; there is a group of diseases like palpebral ptosis, macular dragging in retinopathy of prematurity which preclude using the fovea. The patient has to adopt a chp in order to achieve foveal fixation.
– Neuro-ophthalmological disorders in the form of cerebral diseases affecting supranuclear gaze centers or retinal and optic nerve diseases associated with visual field defects;
– Unknown; in 7% of the ocular torticollis the cause is not identified .
The longstanding ocular problems leading to an abnormal head posture can lead secondarily to a musculoskeletal torticollis, which make difficult the differential diagnosis between ocular and nonocular causes.
Why the children adopt an abnormal/compensatory head posture in certain ophthalmological diseases? The mechanisms involved in improving vision by adopting this new head position are :
1. Improving visual acuity (va): binocular va (certain forms of nystagmus) or monocular va (significant refractive errors, severe restrictive strabismus or infantile esotropia with cross fixation).
2. Maintaining binocular single vision in incomitant strabismus: there is only one gaze position featuring zero or minimal deviation where bifoveal fusion is obtained; the head is moved in such a way to maintain as long as possible this gaze position and binocular single vision. In muscle paralysis there is a head position in which the paretic muscle receives a minimum of impulses to contract. This is the position in which the patient habitually holds the head. As a general rule the head is moving where the eye can’t be moved.
3. Centering the field of binocular vision: monocular patients may turn face to the blind side to put the good eye in the center of the body; children with neurological diseases which cause visual field defects adopt compensatory positions to center the residual visual field with the body (face turn in homonymous hemianopia, chin up or down in altitudinal defects).
4. Other mechanisms: in some incomitant strabismus the head is moved opposite to the side of maintaining binocular vision to maximize separation of the two images and to facilitate suppression or ignoring one image; it is named paradoxical (not compensatory) head posture. For cosmetic reasons some children turn the head to hide an eye deformity (scars, eye deviation, congenital anomalies).
Classification of head postures
According to the three main body axes there are three categories of head orientation:
– Around the antero-posterior axis: the head is tilted to one or the other shoulder;
– Around the vertical axis: the face is turned to one side or the other, away from primary position (straight-ahead gaze direction);
– Around the horizontal axis: the chin is depressed or elevated relative to the primary position;
Some chp are a combination of the three orientations. The term “torticollis” may refer to any head posture, although some authors reserve this term for head tilt.
Ocular causes of head tilt
I. Incomitant strabismus
1) Vertical strabismus (hypertropia, hypotropia). There are innervational or mechanical causes of head tilt:
– Innervational: superior oblique paresis, inferior oblique paresis, inferior rectus paresis, superior rectus paresis, dissociated vertical deviation;
– Mechanical: inferior rectus or superior rectus fibrosis, brown syndrome, orbital floor fracture, thyroid orbitopathy.
Superior oblique paresis (sop) is the most common disorder that leads to ocular chp (12,62% incidence in pediatric ocular chp) and is caused by fourth cranial nerve palsy. Incidence of torticollis in eye muscle palsy (superior oblique, inferior oblique, double elevator, superior rectus, third nerve, sixth nerve) is 33% . There are two forms of sop: congenital and acquired. Congenital sop has an obscure etiology. It is not known if the features are due to a neurogenic palsy or a developmental abnormality of the superior oblique tendon. Direct inspection during surgery and mri examination found redundant, misdirected or absent tendon. In acquired sop, closed head trauma is responsible for most cases.
Diagnosis of sop is based on clinical ophthalmological examination. Checking for eye alignment in all nine diagnostic positions of gaze is highly suggestive (fig. 1). The main sign is hypertropia which means that the affected eye (left eye in fig. 1) Is higher than the congener (or the congener is lower than the affected eye). This sign is visible in primary position (fig. 1.E) and more obvious in adduction (when the involved eye is nasally displaced, seen in fig. 1.A,D,G).
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Figure 1. Clinical ophtamological examination
The explanation is that the superior oblique muscle is a depressor (besides the main action of intorsion) and this action is increased in adduction, so when this muscle is underacting the involved eye goes higher especially in adduction.
Another important clinical sign is the head tilt which is invariable present in unilateral sop. Only sop in a blind eye or bilateral sop may not be associated with chp. Head tilt posture may disappear after occluding one eye and this is a very important characteristic of ocular torticollis. The head tilt can hide hypertropia and predispose to misdiagnosis of the cause of abnormal head posture. In sop the head tilt is usually the dominant posture even if some patients have other components including face turn and/or chin-down. In one series of 59 patients with sop and chp , head tilt was encountered in 46 patients (77,9%), face turn in 39 patients ( 66,1%) and chin-down in only 6 patients (10,1%). In the same study 52,5% of the patients had associated two or all three posture orientations.
The child compensates by tilting the head to the opposite shoulder to minimize the hyperdeviation and maintain fusion (fig. 2A). If the head is tilted to the involved side, hypertropia increases (positive bielschowsky head tilt test, fig. 2B)
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Figure 2. Tilting the head
Congenital sop associates head tilt with facial asymmetry (ocular plagiocephaly ): the hemifacies on the side of the paretic muscle is fuller than the contralateral hemifacies which appears hypodeveloped (fig. 3). This is an important sign which differentiate congenital from acquired sop. The explanation of facial asymmetry is unclear: primary facial hypodevelopment or secondary to the torticollis.
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Figure 3. Facial asymmetry
Without entering in details about surgical procedures, we emphasizes that the treatment of sop involves surgery on one, two or three extraocular muscles, sometimes in both eyes, to reechilibrate the forces between agonists and antagonists. The most preferred surgical procedure is weakening (myectomy or recession) of the inferior oblique on the involved eye and weakening (recession) inferior rectus of the contralateral eye. The earlier the surgery is performed, the less probability for the torticollis to become permanent (secondary musculoskeletal alterations). Figures 4 shows the patient from figure 1 with congenital left sop prior (a) and 5 days after surgery (b) which implied inferior oblique recession on left eye and inferior rectus recession on right eye.
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Figure 4. Five days after surgery
After surgery, hypertropia was absent with the head straight in primary position (fig. 5.C) and minimal in adduction (fig. 5.A, B). Unfortunately, this 9-year old girl with congenital sop has continued to hold the head tilt. Only when the visual demands increase, the head become straight. The success rate for eliminating significant ahp after strabismus surgery for patients with congenital sop is 68.8% In one recent study .
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Figure 5. After surgery
Dissociated vertical deviation (dvd) is characterized by spontaneous, slow upward drift of one eye (fig. 6), Manifested when binocular vision is congenitally affected (infantile esotropia, infantile exotropia). The incidence of dvd in ocular torticollis is approximately 9%. Dvd is accompanied by head tilt in 35-49% of cases [6, 7].
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Figure 6. Slow upward drift of one eye
Some children adopt a head tilt toward the side of the hyperdeviating eye, which recruits otolithic innervations to neutralize dvd and maintain binocular alignment (compensatory head tilting) (fig. 7A). Other children adopt a head tilt to the opposite side (fig. 7B) which is an ancestral postural reflex disclosed by congenital abnormal developmental of binocular cooperation and is noncompensatory for binocular vision but compensatory for vertical orientation of the body .
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Figure 7. Compensatory head tilting
Inferior oblique paresis, inferior rectus paresis, superior rectus paresis are less frequent. Inferior oblique paresis is the rarest of all extraocular muscle paresis. It creates incomitant hypotropia, minimized on tilting the head to the ipsilateral shoulder. It can be congenital or acquired (facial trauma). Inferior rectus paresis can also lead to a head tilt to the ipsilateral side. Superior rectus paresis is associated with head tilt to the contralateral side.
Inferior rectus contracture (fibrosis) with consecutive hypotropia can cause a head tilting to the ipsilateral shoulder which lessens hypotropia. This can be congenital (congenital fibrosis of the extraocular muscles) or arise after blowout fracture of the orbit or, less common in children, in thyroid orbitopathy.
Superior rectus contracture or fibrosis causes hypertropia. It can be idiopathic or secondary to chronic superior oblique paresis or thyroid orbitopathy and is associated with head tilt to the contralateral shoulder where the hypertropia lessens.
Brown syndrome is caused by a mechanical restriction (congenital or acquired) of the superior oblique tendon moving through the trochlea, which result in a restriction of elevation of the eye in adduction (fig. 8).
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Figure 8. Restriction of elevation of the eye in adduction
Unilateral brown syndrome may cause ipsilateral head tilt but more frequent (fig. 9) Or chinup. Torticollis incidence is around 30% . The treatment is surgical by weakening the tendon of the superior oblique (tenotomy).
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Figure 9. Contralateral face turn
2) Horizontal strabismus (esotropia – strabismus with convergent axes, exotropia – strabismus with divergent axes) and especially esotropia can be associated with head tilt but usually is the associated nystagmus that cause the compensatory head posture not the eye deviation itself. However, there are other cases where nystagmus is absent and esotropia differs on right versus left tilt. The patient will adopt the head tilt to the side with less esodeviation.
3) Torsional strabismus (cyclotropia) has two forms: excyclotropia which is a temporal rotation of the superior portion of the vertical eye meridian and incyclotropia which is a nasal rotation of the vertical eye meridian. Head tilt is a compensatory sensorial mechanism to align this meridian with the body vertical axis. For example, when the right eye is excyclotropic, the head is tilted to the left shoulder. In sop, when excyclotropia is associated to hypertropia, the head tilt position is adopted because of the vertical rather than the torsional misalignment .
Nystagmus can lead to any head posture. The incidence of all types of nystagmus in pediatric ocular torticollis is 21,36%. Head tilt as the only abnormal head posture in nystagmus is rare. More frequent is associated with face turn or / and chin-up or down. The nystagmus intensity decreases when the head is tilted toward one shoulder, whereas it increases on tilting to the opposite shoulder. The most frequent cause of head tilt is spasmus nutans syndrome. This is a triad of a fine, rapid frequency nystagmus with head nodding and chp. It is usually benign, with onset in the first year of life and remission by age 3 or 4. It is not associated with neurological abnormalities but neurological examination is mandatory to exclude any cerebral pathology associated to spasmus nutans – like picture. Infantile nystagmus syndrom, infantile esotropia with latent nystagmus are other entities associated in rare occasions with head tilt.
III. Refractive errors
Refractive errors are encountered in 2,91% of pediatric ocular torticollis. Uncorrected or undercorrected refractive errors can cause head tilt. A high astigmatism in the fixating eye can induce a head tilt when axis of the cylinder is oblique. The correction of the astigmatism alleviates the posture. In lens subluxation, which is a frequent finding in marfan syndrome, the patient may adopt a head tilt position to improve refractive correction and consecutively, visual acuity.
Ocular causes of chin-down
Chin-up and chin-down postures as forms of ocular torticollis, are less prone to confusion with nonocular torticollis in opposition to head tilt and face turn postures.
I. Incomitant strabismus
1) ”A” and “v”-pattern strabismus are clinical forms of horizontal strabismus characterized by increase or decrease of the deviation from the midline position (primary position) in upgaze as compared with downgaze. The incidence of a and v-patterns in pediatric ocular torticollis is 7,76%. The presence of chp depends on the nature of the underlying strabismus and the size of the deviation. If the deviation is present in primary position, the child may assume a chinup or chin-down posture in order to fuse and obtain binocular vision. If the deviation is absent in primary position, no chp will appear.
The diagnosis of pattern strabismus is not easy to do, especially when chp is present. The chp may hide the deviation and the parents frequently will not notice the underlying strabismus. More, they may perceive the chin-down position of the head as a sign of shyness of her or his child. Incidence of chp in pattern strabismus is 19%.
The etiology of pattern strabismus is not fully elucidated. More than one factor is implicated: oblique muscle dysfunction (overaction, sagittalization), orbital structural anomalies (pulley heterotopia of the extraocular rectus muscles, mongoloid or antimongoloid palpebral fissure), craniofacial syndromes (crouzon or apert).
V-pattern esotropia or an a-pattern exotropia are associated with chin-down posture. This is because chin-down posture forces the patient to look in upgaze position where the deviation (exo in a-exotropia and eso in v-esotropia) is minimal or even absent.
V-pattern esotropia is characterized by maximal esodeviation in the downgaze field, whereas it decreases progressively as the eyes move up to midline position and into the upgaze field. In upgaze esotropia may disappear and orthotropia is installed (fig. 10).
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Figure 10. V-pattern esotropia
V-esotropia is the most frequent pattern strabismus and is usually associated with infantile esotropia and inferior oblique overaction or with bilateral superior oblique paresis. Antimongoloid palpebral fissure slant (fig. 13) Is a clinical sign when orbital structural anomalies are associated. Surgery consists in weakening the inferior obliques by recession or myectomy on both eyes, with or without rectus muscles procedures (weakening and insertion transposition). The 6-year-old girl from figure 11. A with v-esotropia was operated on both eyes: inferior oblique myectomy and medial rectus inferior transposition. After surgery (b) orthotropia in all vertical positions of gaze is achieved. The chp has disappeared.
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Figure 11. V-esotropia before and after surgery
A-pattern exotropia is characterized by maximal exodeviation in the downgaze field, whereas it decreases progressively as the eyes move up to midline position and into the upgaze field. In upgaze exotropia may disappear and orthotropia is seen (fig. 12). A-exotropia is encountered in superior oblique overaction, inferior oblique paresis, orbital structural changes with mongoloid slant of the palpebral fissures or horizontal muscle pulley heterotopy. Surgery consists in weakening the superior obliques by recession or tenotomy on both eyes, with or without rectus muscles procedures (weakening and insertion transposition). The 6-year-old girl from figure 12 (a) with a-exotropia was operated on both eyes: superior oblique recession and lateral rectus inferior transposition. Postoperative aspect (b) shows orthotropia in all vertical positions of gaze. The chp has disappeared.
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Figure 12. Orthotropia before and after surgery
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Figure 13. Antimongoloid palpebral fissure slant
2) Vertical strabismus. Any disease which cause uniocular or binocular depression deficit may induce chin-down posture. There are innervational and mechanical causes:
– Innervational: superior oblique (fourth nerve) paresis, inferior rectus (partial third nerve) paresis. Unilateral paresis of either muscle can cause hypertropia in primary position which is smaller or absent in upgaze. The fusion and binocular single vision is possible only in upgaze field, so, the child has to adopt a chin-down position as chp. In figure 3a, the patient with right sop has head tilt and chin-down posture as chp. Paresis of the inferior rectus is very rare. When both muscles are affected (usually after orbital trauma) the term is “double depressor paresis”.
– Mechanical: superior rectus or inferior oblique restrictions, caused by orbital roof fracture, scars or thyroid orbitopathy are extremely rare in children.
Infantil nystagmus syndrome can lead to any head posture. If the null zone is localized in upgaze field, then the child may adopt a chindown position to ameliorate the binocular visual acuity.
There are also acquired forms of nystagmus (after lower brainstem lesions) associated with the null zone in upgaze position.
Uncorrected or undercorrected refractive errors may predispose to chin-down position to improve visual acuity, especially hyperopia .
Neuro-ophthalmological diseases may cause chp by direct involvement of the ocular motility or by alteration of the visual field. Damage to the vertical gaze centers (rostral interstitial nucleus of the medial longitudinal fasciculus) by tumors, trauma or inborn errors of metabolism (gaucher, nieman-pick diseases), can lead to downgaze paresis. If the eyes are not able to move down, then the head will be moved down to improve visual comfort.
Retinal or optic nerve diseases which cause altitudinal inferior visual field defect are associated with chin-down posture to centralize the residual field with the body.
Ocular causes of chin-up
I. Incomitant strabismus
1) ”A” and “v”-pattern strabismus.
The two entities which may be associated with chin-up posture are v-exotropia and a-esotropia. This is because chin-up posture forces the patient to look in downgaze position where the deviation (exo in v-exotropia and eso in a-esotropia) is minimal or even absent.
V-exotropia is characterized by maximal exodeviation in upgaze field which decrease in midline position and is minimal or even absent (orthotropia) in downgaze field (fig. 13). Antimongoloid palpebral fissure slant is sometimes associated. The etiology and surgical treatment are the same like in v-esotropia excepting the association with exotropia which imply another strategy on rectus muscle surgery (weakening procedure and insertion transposition of the lateral rectus muscles).
A-esotropia is characterized by maximal esodeviation in upgaze field which decrease in midline position and is minimal or even absent (orthotropia) in downgaze field (fig. 14). The etiology and surgical treatment are the same like in a-exotropia excepting the association with esotropia which imply another strategy on rectus muscle surgery (weakening procedure and insertion transposition of the medial rectus muscles).
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Figure 14. A-esotropia
2) Vertical strabismus. Any disease which causes uniocular or binocular elevation deficit may induce chin-up posture. There are innervational and mechanical causes:
– Innervational: inferior oblique or superior rectus (partial third nerve) paresis. Unilateral paresis of either muscle can cause hypotropia in primary position which is smaller or absent in downgaze. The fusion and binocular single vision is possible only in downgaze field, so, the child has to adopt a chin-up position as chp. When both muscles are involved (affected inferior division of the third nerve) the term is “double elevator paresis”. Treatment involves surgical procedures of weakening (recession) inferior rectus muscle and/or strengthening (resection) superior rectus muscle on the hypotropic eye.
– Mechanical: brown syndrome, inferior rectus or inferior oblique restrictions caused by congenital fibrosis syndromes, orbital floor fractures (much common than the roof fractures), postoperative or posttraumatic scars or thyroid orbitopathy. Treatment is specific to each etiology.
Congenital fibrosis of extraocular muscles (cfeom) is part of ccdds. It result from primary abnormality at the oculomotor (third) and trochlear (fourth) nucleus and nerve levels. The most common clinical signs are bilateral infraducted (depressed) eye with restricted upgaze, bilateral ptosis and chin-up posture. The management of strabismus is difficult because is large and needs very large recessions and occasionally resections of the inferior and superior rectus muscles.
Infantil nystagmus syndrome can lead to any head posture. If the null zone is localized in downgaze field, then the child may adopt a chin-up position to ameliorate the binocular visual acuity.
Acquired diseases (dorsal midbrain syndrome) that cause vertical nystagmus exaggerated in upgaze field may lead to chin-up posture to optimize visual acuity.
III. Palpebral ptosis
Palpebral ptosis is an important causes of ocular torticollis in children with an incidence of 9,7%. Congenital ptosis may be isolated (most frequent) as figure 15 or associated in syndromes: blepharophimosis syndrome, congenital fibrosis of the extraocular muscles. Acquired ptosis associated with chp is rare in children. No matter if ptosis is congenital or acquired, unilateral or bilateral, it will be associated with chin-up when the lid margins are at or below the level of the pupil. Incidence of chp in ptosis is 7%. This posture is adopted to clear the visual axis and to improve unilateral or bilateral visual acuity.
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Figure 15. Congenital ptosis
IV. Refractive errors
Uncorrected or undercorrected refractive errors may predispose to chin-up posture to create a narrowed palpebral fissure which act like a stenopeic slit, improving image clarity. This is particularly useful in myopia and astigmatism.
V. Neuro-ophthalmological diseases
Neuro-ophthalmological diseases may cause chp by direct involvement of the ocular motility or by alteration of the visual field. Damage to the vertical gaze centers from dorsal rostral midbrain can lead to upgaze paresis. Dorsal midbrain syndrome results from lesions at the posterior commissure in the dorsal rostral midbrain like hydrocephalus, tumors, stroke, inborn errors of metabolism, encephalitis. It includes paresis of upgaze, nystagmus (which also contributes to the chin-up posture), eyelid retraction and light-near dissociation of the pupils. If the eyes are not able to move up, then the head will be moved up to improve visual comfort. Retinal or optic nerve diseases which cause altitudinal superior visual field defect are associated with chin-up posture to centralize the residual field with the body.
Refer from website: http://www.jpss.eu/index.php/future-meetings/item/659-understanding-ocul…
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