Ординатура / Офтальмология / Английские материалы / Manual of Squint_Ahuja_2008
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Paralytic Squints |
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TABLE 11.2: Difference between ocular and congenital torticollis |
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Ocular Torticollis |
Congenital torticollis |
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1. |
— |
1. Marked resistance to passive |
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straightening of the head |
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2. |
— |
2. Often, a fibroma mass may be felt in |
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the contracted sternomastoid muscle |
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3. |
Patching (occlusion) of the paretic |
3. Patching has no effect on congenital |
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muscle can relive ocular torticollis, |
torticollis |
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provided no secondary) skeletal or |
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muscular changes have developed |
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in the neck |
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TABLE 11.3: Differential diagnosis between congenital and acquired palsy |
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Congenital |
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Acquired |
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1. |
Intermittent diplopia |
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(A) |
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2. |
Intermittent squint |
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(A) |
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3. |
Head posture but patient is unaware of this |
(A) |
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4. |
Anatomical changes in vertebral column |
(A) |
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5. |
Suppression is usually present |
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(A) |
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TOTAL OPHTHALMOPLEGIA
Inv. of Extrinsic, ocular muscle
Intrinsic ocular muscle
IPS
Ptosis+
Proptosis+
Ocular movement (A) or restricted
Pupillary activity to light
Accommodation and convergence (A)
DOUBLE DEPRESSOR PARALYSIS
Double depressor paralysis is a rare anomaly and it consists of inability to depress the eye from primary position, adduction or abduction. This is caused by long-standing paralysis of the inferior rectus muscle rather by paralysis of both inferior rectus and superior oblique muscle (Table 11.4).
Botulinum Toxin
In paralytic strabismus, the botulinum induced paralysis of the antagonist muscle prevents or reduces its contracture during spontaneous recovery of the paretic muscle. Also, as the initial overaction resulting from the injection slowly resolves and the eyes approach the primary position, fusion may “lock on” resulting in Orthophora.
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Manual of Squint |
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TABLE 11.4: Differential diagnosis between paralytic and nonparalytic squint |
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Paralytic |
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Nonparalytic |
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1. |
Eyes move in such an |
1. |
Eyes move in coordinated manner |
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incoordinated manner so |
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and angle of squint remain same in |
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that the angle of squint varies |
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all direction of gaze |
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in different direction of gazes |
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and on changing fixation from |
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one to other eye. |
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2. |
Diplopia is a prominent feature |
2. |
No. diplopia |
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3. |
Nausea and vertigo |
3. |
(A) |
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4. |
Compensatory head posture |
4. |
(A) |
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5. |
Onset – sudden |
5. |
Usually in children |
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6. |
Amblyopia, supervision, ARC, |
6. |
Amblyopia, supervision, ARC, |
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eccentric fixation absent |
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eccentric fixation present |
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7. |
Secondary deviation/primary |
7. |
Secondary = Primary deviation |
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deviation |
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8. |
Some changes present in |
8. |
Not so |
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uninvolved muscle |
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9. |
Palliative treatment is required |
9. |
No palliative treatment |
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10. |
Wait for 6-8 months for surgery |
10. |
Immediate it is required |
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The advantages of botulinum toxin therapy for strabismus are: (1) it can be performed on an outpatient basis, (2) it carries minimum risk,
(3) leaves no scar, (4) can be used for postoperative residual strabismus and (5) can be used when surgery is inappropriate. It has been shown in paralytic strabismus toxin have better chance of recovery than those that have not been treated. In lateral rectus palsy contacture of the antagonist medial rectus muscle can be prevented and this should make subsequent elective surgery easier.
The disadvantages of botulinum toxin therapy for strabismus are:
(1) more than two injection is often needed to determine the optimum dose to obtain maximal benefit, (2) alignment changes are not as stable as with surgery and (3) transient partial ptosis and vertical strabismus frequently occur. There is dramatic relief of symptoms following treatment with botulinum toxin.
The other reported complication of botulinum therapy are: (1) scleral perforation, (2) retrobulbar hemorrhages, (3) diplopia, (4) pupillary dilatation, (5) ecchynosis, (6) corneal exposure, (7) ptosis, (8) ectropon,
(9)lagophthalmos and (10) chemosis.
Botulinum toxin is curative in some cases of paralytic strabismus, in
others it prevent contracture of the antagonist and should therefore make subsequent surgery simple.
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APPLIED ANATOMY
Oculomotor Nerve (IIIrd N) (Fig. 12.6)
The oculomotor or the IIIrd cranial nerve innervates all the extraocular muscles except the lateral rectus and the superior oblique. In addition, it carries the parasympathetic fibers to the ciliary muscle and the sphincter pupillae. The nucleus of IIIrd nerve is in the form of a complex formed by a number of subnuclei and is situated in the midbrain) at the level of superior colliculi. Below the aqueduct of Sylvius. The subnuclei include:
i.Subnucleus for levator: It lies in the caudal part of the complex and is unpaired, thus supplying levator muscle of the lids of both eyes. Therefore, a lesion confined to this area will lead to ptosis of both eyes.
ii.Subnucleus for superior rectus: This is paired, and supplies the contralateral superior rectus muscle. This implies that in a case of IIIrd nerve palsy, if the contralateral superior rectus has been spared, the lesion does not lie in the nucleus.
iii.Subnucleus for medial rectus, inferior rectus and inferior oblique: This is also a paired group of cells, supplying the corresponding muscles of the same (ipsilateral) side.
iv.Accessory nucleus: Situated posterior to the main mass, it sends preganglionic parasympathetic fibers along the motor fibers, and is related to the phenomenon of near reflex, accommodation, and
perhaps, convergence (Perlia’s nucleus).
In general, it is rare to see lesions purely localized in the nuclear complex. Certain vascular lesion, demyelinating diseases and tumors may involve this region.
The efferent fibers from the complex form the fasciculus, which travel through the red nucleus and medial part of the cerebral peduncles, emerging from midbrain. Lesions in this zone are caused by the same conditions as in the case of nuclear complex, and may lead to two wellrecognized syndromes:
Benedikt’s syndrome: This is characterized by an ipsilateral IIIrd nerve palsys and a contralateral hemiplegia with tremors. This is the result of lesions of the fasciculus in the red nucleus.
Weber’s syndrome: This caused by the fascicular lesion in the cerebral peduncles, and is characterized by an ipsilateral IIIrd nerve palsy accompanied by a contralateral hemiparesis.
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The basilar part of the nerve is constituted by 15-20 rootlets in the interpeduncular area which join one another to form the main trunk.
The main trunk of the nerve is flattened at the beginning, twists around to bring the inferior fibers superiorly and assumes a rounded shape. It travels between the posterior cerebral and superior cerebellar arteries. Further forwards, it lies lateral and parallel to the posterior communicating artery, reaching the cavernous sinus. During this course, as it traverses the base of skull, it is unaccompanied by any other cranial nerve. It is, therefore, quite common to see isolated palsy of the third nerve in the basilar part, caused by aneurysms or head injuries.
A painful IIIrd nerve palsy with pupillary involvement is typically seen in the aneurysms at the junction of the posterior communicating artery and the internal carotid artery (Fig. 11.6).
In a case of extradural hematoma following head injury, a pressure may result leading to herniation of the temporal lobe. This compresses the third nerve over the tentorial edge, manifesting initially as a dilated and fixed pupil followed by a total palsy of the nerve.
The intracavernous part, the nerve enters the cavernous sinus by piercing the dura in its posterior part just lateral to the posterior clinoid processes, lying superior to the trochlear nerve.
In the anterior part, it divides into superior and inferior division and enters the orbit via the middle portion of superior orbital fissure within the annulus of Zinn.
FIG. 11.6: Anatomy of IIIrd nerve
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Cavernous sinus lesions such as aneurysms, carotidcavernous fistula, Tolosa-Hunt syndrome may cause IIIrd nerve palsy in association with palsy of other nerves within the cavernous sinus, i.e. the IVth nerve and the first division of Vth nerve. The pupil usually remains unaffected. Diabetes is another important condition that may cause a vascular palsy of the IIIrd nerve.
The intraorbital part, the nerve enters the orbit after dividing into a superior division (supplying the levator and superior rectus), and inferior division (supplying medial rectus, inferior rectus and inferior oblique) muscles. The inferior division also carries parasympathetic fibers from Edinger-Westphal nucleus to sphincter pupillae and the ciliary muscle.
The nature of blood supply to the third nerve has important clinical bearings. While the pupillomotor fibers located in the median and superior part of the third nerve is nourished by the pial vessels, the main trunk derives its blood via vasa nervosum. The surgical conditions like aneurysms and head injury compress the pial vessels leading to the paralysis of pupillomotor fibers. On the other hand, medical conditions like diabetes and hypertension primarily affect the vasa nervosum and so, the pupillomotor fibers may be spared (Fig. 11.7).
THE TROCHLEAR NERVE (IVTH N)
This is the longest and the thinnest of all cranial nerves. It is purely a motor nerve innervating the superior oblique muscle of the opposite side. It is also peculiar in that it emerges out from the dorsal aspect of the brain.
FIG. 11.7: Location of pupillomotor fibres in IIIrd nerve
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The nucleus of trochlear nerve lies in the midbrain at the level of inferior colliculi, and is in continuation with the nucleus of IIIrd nerve.
The fascicular component is constituted by the axons that curve around the aqueduct of Sylvius and decussate completely.
The trunk (precavernous part), emerges on the dorsal aspect of the midbrain and curves forward between the posterior cerebral and the superior cerebellar runs arteries as does the trunk of IIIrd nerve. It pierces the dura below the IIIrd nerve to enter the posterior part of cavernous sinus. The infracavernous part lies in the lateral wall of the sinus below the third nerve and above the first division of Vth nerve. In the anterior part, it crosses over the IIIrd nerve and enters the orbit through lateral part of the superior orbital fissure, superotemporal to the annulus of Zinn.
The intraorbital part carries the nerve supply to the superior oblique muscle.
THE ABDUCENS NERVE (VITH N)
The VIth cranial nerve is motor in function, has a long course and innervates the lateral rectus muscle of the same side.The nucleus of sixth nerve lies in the middle of pons below the fourth ventricle and is closely associated with the fasciculus of the facial nerve. In addition, it is also connected with the pretectal nucleus of both sides as well as the horizontal gaze center in the pontine paramedial reticular formation. Therefore, any lesion affecting the zone of VIth nerve. Nucleus will not cause an isolated paralysis of the ipsilateral lateral rectus muscle, but will be accompanied by:
i.Paralysis of conjugate movements towards the side of lesion
ii.Ipsilateral facial nerve palsy, by way of the involvement of fasciculus
of facial nerve.
The fascicular part is composed of the axons emerging from the nucleus, pass forwards through the medial meniscus and the pyramidal tract leaving the brainstem at the junction of pons and midbrain, lateral to the pyramidal prominence. In view of its course through the pyramidal tract and medial meniscus. A lesion in the region of fascicule is likely to cause multiple clinical manifestations in the form of Foville’s syndrome. This is manifested if the lesion is located at the site where the fasciculus traverses the medial meniscus, and shows:
•Paralysis of the ipsilateral lateral rectus muscle, paralysis of the lateral gaze
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•Paralysis of the lateral gaze towards the same side
•Facial weakness (damage to the facial nerve nucleus)
•Facial analgesia (damage to the sensory portion of Vth nerve)
•Homer’s syndrome
•Deafness.
Millard-Gubler syndrome. The lesion at the sight of the fasciculus passing through the pyramidal tract will be characterized by paralysis of the ipsilateral lateral rectus muscle.
Contralateral Hemiplegia
The basilar portion of the nerve, after emerging from the pontomedullary junction, passes upwards close to the base of the pons and is crossed by the anterior inferior cerebellar artery. It runs further upwards on the back of petrous temporal bone near its apex turning sharply at right angle on the sharp border of the petrous bone before piercing the dura to enter the cavernous sinus, lateral to the dorsum sellae. Damage to the basilar portion may occur in the following situations:
i.Acoustic neuroma: This tumor located at the cerebellopontine angle may cause damage to multiple cranial nerves, viz. the Vth, VIth, VIIth, and VIIIth nerves. Therefore, paralysis of the lateral rectus in such cases is accompanied by a hearing loss which is the first symptom, and loss of corneal sensation which is the first sign (i.e. it precedes the VIth nerve involvement).
ii.Nasopharyngeal tumors: Following the invasion of skull and its foramina, these tumors can damage the VIth nerve in it basilar course.
iii.Raised intracranial pressure (Fig. 11.8): The increased pressure, especially in case of posterior fossa tumors or in benign intracranial hypertention (pseudotumor cerebri) tends to push the brain downwards. Such a movement may damage the VIth nerve on stretching at the sharp border of petrous bone where it makes a sharp right angled turn. The nerves may be damaged on both the sides. The resultant VIth nerve palsy, however, has no localizing value.
iv.Basal skull fracture: Damage to the VIth nerve (unilateral or bilateral)
in this situation is nonspecific, and may be a part of the overall damage to the brain tissue.
The infracavernous part of the nerve lies below the IIIrd and IVth nerve, as well as the first division of the Vth nerve, placed most medially
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Fig. 11.8: Mechanism of bilateral VIth nerve palsy resulting from raised intraocular pressure
and close to the internal carotid artery, thus rendering it more vulnerable than other nerves. It also carries the sympathetic fibers from the paracarotid plexus and thus a paralysis of the intracavernous portion of the nerve may be associated with a postganglionic Homer syndrome (Parkinson sign).
The nerve gets involved by the same set of lesions involving the IIIrd and the IVth nerve inside the cavernous sinus.The infraorbital part of the nerve begins with its entry to the orbit through the annulus of Zinn, and innervates the lateral rectus muscle.
12 Vertical Strabismus
As in the case of horizontal deviations, a vertical squint can be concomitant or incomitant (congenital or acquired). It may express itself in the form of a hyperphoria, intermittent hypertropia, or a (constant) hypertropia. Depending upon the eye involved, it may be right hypertropia or left hypertropia.
COMITANT VERTICAL DEVIATIONS
It is not uncommon to see such type of deviations, either in an isolated form or in association with horizontal deviations. The underlying cause is not well-understood. Some form of innervational disturbance may be a likely factor. In many instances, it may be the result of a paralytic incomitant hyperdeviation attaining the character of a comitant deviation over a long period of time. The common features of such deviations are as follows:
i.Intermittent hypertropia is more common than a constant deviation
ii.Suppression, amblyopia or a vertical anomalous retinal correspondence may be present
iii.Small vertical deviations are typically present in association with moderate to large horizontal deviations
iv.Many cases demonstrate an under or over action of one or more cyclovertical muscles.
Treatment
Orthoptic treatment is directed to treat amblyopia. In small deviations upto 15 prism diopters, prisms are provided to neutralize the deviation. The power of prism is equally divided in two eyes with the base down in front of the hypertropic eye and base up in the other eye.
Surgical treatment is planned on the basis of the amount of deviation, and the presence of associated horizontal deviations. In small deviations
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combined with horizontal deviation, a correction of the vertical element may be achieved by shifting the insertion of the horizontal muscle (5-8 mm) in the hypertropic eye, or shifting it up (to the same amount) in the hypotropic eye.
In large deviations, a recession of superior rectus of the hypertropic and recession of inferior oblique of the other eye is indicated.
DISSOCIATED VERTICAL DEVIATIONS (DVD)
It is basically a bilateral anomaly characterized by the hyperdeviation of either eye when the other eye is fixing. The hyperdeviation is accompanied by extortion and slight exodeviation. In this situation, if the fixing eye is covered, the squinting eye takes up fixation by moving down and in along with intortion. But, the covered eye does not make any movement, thus defying the Hering’s law of ocular movements. That is why this type of vertical deviation is prefixed with the term ‘Dissociated. It may be associated with any type of strabismus, any anomaly of binocular vision, nystagmus, or any defect ocular movements. On the other hand, it is seen as an isolated form. The etiology of this neuromuscular anomaly has not been explained clearly. Features—DVD is characterized by:
i.A spontaneous occurrence of vertical deviation of either eye when the patient is fatigued, or when fusion is interrupted by artificial means such as covering one eye.
ii.Lack of subjective symptoms in majority of case, an intermittent deviation being noticed by the onlookers—friends or parents. Some cases may have asthenopic symptoms. Diplopia is rare.
iii.Its frequent association with other forms of strabismus, specially with essential congenital exotropia and essential exotropia.
iv.Suppression in the nonfixing eye is present to eliminate diplopia.
v.Presence of peripheral fusion if there is no associated horizontal deviation.
vi.Presence of a facultative absolute scotoma, though bilateral, manifesting in the nonfixing eye.
vii.A frequent presence of latent nystagmus in cases of alternate DVD.
Diagnosis
The diagnosis of DVD is made on a careful assessment of the following tests.