PARALYTIC STRABISMUS

It refers to ocular deviation resulting from complete
or incomplete paralysis of one or more extraocular
muscles.
Etiology
The lesions may be neurogenic, myogenic or at the
level of neuromuscular junction.
I. Neurogenic lesions
1. Congenital. Hypoplasia or absence of nucleus is
a known cause of third and sixth cranial nerve
palsies. Birth injuries may mimic congenital
lesions.
2. Inflammatory lesions. These may be in the form
of encephalitis, meningitis, neurosyphilis or
peripheral neuritis (commonly viral). Nerve trunks
may also be involved in the infectious lesions of
cavernous sinus and orbit.
3. Neoplastic lesions. These include brain tumours
involving nuclei, nerve roots or intracranial part
of the nerves; and intraorbital tumours involving
peripheral parts of the nerves.
4. Vascular lesions. These are known in patients
with hypertension, diabetes mellitus and
atherosclerosis. These may be in the form of
haemorrhage, thrombosis, embolism, aneurysms
or vascular occlusions. Cerebrovascular accidents
are more common in elderly people.
5. Traumatic lesions. These include head injury
and direct or indirect trauma to the nerve trunks.
6. Toxic lesions. These include carbon monoxide
poisoning, effects of diphtheria toxins (rarely),
alcoholic and lead neuropathy.
7. Demyelinating lesions. Ocular palsy may occur
in multiple sclerosis and diffuse sclerosis.
II. Myogenic lesions
1. Congenital lesions. These include absence,
hypoplasia, malinsertion, weakness and musculofacial
anomalies.
2. Traumatic lesions. These may be in the form of
laceration, disinsertion, haemorrhage into the
muscle substance or sheath and incarceration of
muscles in fractures of the orbital walls.
3. Inflammatory lesions. Myositis is usually viral in
origin and may occur in influenza, measles and
other viral fevers.
4. Myopathies. These include thyroid myopathy,
carcinomatous myopathy and that associated with
certain drugs. Progressive external ophthalmoplegia
is a bilateral myopathy of extraocular
muscles; which may be sporadic or inherited as
an autosomal dominant disorder.
III. Neuromuscular junction lesion
It includes myasthenia gravis. The disease is
characterised primarily by fatigue of muscle groups,
usually starting with the small extraocular muscles,
before involving other large muscles.
Clinical features
Symptoms
1. Diplopia. It is the main symptom of paralytic
squint. It is more marked towards the action of
paralysed muscle. It may be crossed (in divergent
squint) or uncrossed (in convergent squint). It
may be horizontal, vertical or oblique depending
on the muscle paralysed. Diplopia occurs due to
formation of image on dissimilar points of the two
retinae (Fig. 13.23).
2. Confusion. It occurs due to formation of image of
two different objects on the corresponding points
of two retinae.
3. Nausea and vertigo. These result from diplopia
and confusion.
4. Ocular deviation. It is of sudden onset.
Signs
1. Primary deviation. It is deviation of the affected
eye and is away from the action of paralysed
muscle, e.g., if lateral rectus is paralysed the eye
is converged.
2. Secondary deviation. It is deviation of the normal
eye seen under cover, when the patient is made
to fix with the squinting eye. It is greater than the
primary deviation. This is due to the fact that the
strong impulse of innervation required to enable
the eye with paralysed muscle to fix is also
transmitted to the yoke muscle of the sound eye
resulting in a greater amount of deviation. This is
based on Hering’s law of equal innervation of
yoke muscles.
3. Restriction of ocular movement. It occurs in the
direction of the action of paralysed muscles
4. Compensatory head posture. It is adopted to
avoid diplopia and confusion. Head is turned
towards the direction of action of the paralysed
muscle, e.g., if the right lateral rectus is paralysed,
patient will keep the head turned towards right.
5. False projection or orientation. It is due to
increased innervational impulse conveyed to the
paralysed muscle. It can be demonstrated by
asking the patient to close the sound eye and
then to fix an object placed on the side of
paralysed muscle. Patient will locate it further
away in the same direction. For example, a patient
with paralysis of right lateral rectus will point
towards right more than the object actually is.
Pathological sequelae of an extraocular muscle
palsy
In all cases of extraocular muscle palsy, certain
sequelae take place after some time. These occur more
in paralysis due to lesions of the nerves than the
lesions of muscles. These include:
1. Overaction of the contralateral synergistic muscle.
2. Contracture of the direct antagonist muscle.
3. Secondary inhibitional palsy of the contralateral
antagonist muscle.
For example, in paralysis of the right lateral rectus
muscle there occurs (Fig 13.24):
Overaction of the left medial rectus,
Contracture of the right medial rectus and
Inhibitional palsy of the left lateral rectus muscle.
Clinical varieties of ocular palsies
1. Isolated muscle paralysis. Lateral rectus and
superior oblique are the most common muscles to be
paralysed singly, as they have separate nerve supply.
Isolated paralysis of the remaining four muscles is
less common, except in congenital lesions.
2. Paralysis of the third cranial nerve. It is of
common occurrence. It may be congenital or acquired.
Clinical features of third nerve palsy (Fig. 13.25 A
and B) include:
Ptosis due to paralysis of the LPS muscle.
Deviation. Eyeball is turned down, out and slightly
intorted due to actions of the lateral rectus and
superior oblique muscles.
Ocular movements are restricted in all the
directions except outward.
Pupil is fixed and dilated due to paralysis of the
sphincter pupillae muscle.
Accommodation is completely lost due to
paralysis of the ciliary muscle.
Crossed diplopia is elicited on raising the eyelid.
Head posture may be changed if pupillary area
remains uncovered.
3. Double elevator palsy. It is a congenital condition
caused by third nerve nuclear lesion. It is
characterised by paresis of the superior rectus and
the inferior oblique muscle of the involved eye.
4. Total ophthalmoplegia. In this condition all
extraocular muscles including LPS and intraocular
muscles, viz., sphincter pupillae, and ciliary muscle
are paralysed. It results from combined paralysis of
third, fourth and sixth cranial nerves. It is a common
feature of orbital apex syndrome and cavernous sinus
thrombosis.
5. External ophthalmoplegia. In this condition, all
extraocular muscles are paralysed, sparing the
intraocular muscles. It results from lesions at the level
of motor nuclei sparing the Edinger-Westphal
nucleus.
6. Internuclear ophthalmoplegia. In this condition
there is lesion of the medial longitudinal bundle. It is
the pathway by which various ocular motor nuclei
are linked. Internuclear ophthalmoplegia is
characterised by: defective action of medial rectus
on the side of lesion, horizontal nystagmus of the
opposite eye and defective convergence.