Case of the week 42.html

In any strabismus case , we have to follow the rules :

Definitely , we are dealing with a case of non-comitant strabismus since the angle of deviation isn't the same in different gazes .

The presence of diplopia , abnormal head posture , together with the absence of mechanical restrictive orbital pathology ( normal MRI ) , mean that we are definitely dealing with a case of paralytic strabismus .

A paralytic hyperdeviation is usually difficult to diagnose because we have to differentiate between a pair of elevators or depressors in each eye. As in this case there is a left hypertropia in primary position , this means the following possibilities :

         a. Paralysis of one of the depressors of the left eye
        b. paralysis of one of the elevators of the right eye

         ( Left IR , Left SO       Vs       Right SR , Right IO )

it must be recognized whether the hypertropia is greater on right or left gaze. If the left hypertropia increases in left gaze , as we are seeing here , this may be caused by paralysis of the left inferior rectus or the right inferior oblique muscles.

In patients who have a paresis of longer standing, as in our patient , the head tilt test could be used to differentiate between a paretic elevator muscle in one eye and a paretic depressor muscle in the other.

As we see , the left hypertropia is greater on head tilt to the right shoulder ( the opposite side of the hypertropia ) , Keeping all this in mind with the Park’s 3 step test this means that this patient has definitely an isolated left inferior rectus paralysis .

When the paralysis is of recent onset, the diagnosis is made on the basis of incomplete duction in the field of action of the suspected rectus or oblique muscles , this makes the differentiation is usually easy . However, it is a common mistake in recent paralysis to depend on the examination of ductions to confirm a paresis of a specific muscle , since the patient may overcome the muscle weakness by maximal innervational effort when fixating with the paretic eye. More revealing is the examination of versions, for under these circumstances the patient will show marked overaction of the yoke muscle of the paretic muscle in the contralateral eye when fixating with the paretic eye.

In long standing IR paralysis - as in our patient - the prominent motility feature is the overaction of the antagonist of the paralyzed muscle i.e the left SR ( see the marked hypertropia on looking left-up gaze , picture 3 ) .

Finally , concerning the head posture , Anomalies of head posture should alert the ophthalmologist to the presence of paralytic strabismus, this sign is of limited value in ascertaining the nature of the underlying pathology except with paralysis of the oblique muscles. In these conditions of oblique muscle palsy , the head is inclined toward the opposite side in superior oblique paralysis and toward the paretic side in inferior oblique paralysis , although a head tilt toward the paralyzed side ( paradoxical head tilt ) may occur occasionally with paralysis of the superior oblique muscle. The direction of compensatory head position varies more frequently with paralysis of the vertical rectus muscles, when the head may be tilted toward the involved or noninvolved side .

On Further clinical evaluation FDT test is assumed to be negative for any superior rectus pathology. This is likely in this case as I already mentioned that there is a normal MRI and no real thickening of the superior rectus muscle.

Thyroid Eye Disease
Trauma with or without fracture floor of orbit
Extra-ocular muscle cysticercosis
Myositis
Midbrain Infarct
Ocular Myasthenia

Keeping in mind the details available in my case , in a 26 years old male with an acute onset of inferior rectus paralysis the more likely causes are Post- traumatic , myositis or an idiopathic .

Most of these causes however will have a definite history of pain, redness ,watering at some time or other .

EOM myositis is however less likely as there is no tendon involvement as mentioned before in the details .

Thyroid eye disease may also have an insidious onset and there is a predilection for Medial Rectus and inferior rectus involvement in these cases. However, patients may be euthyroid on systemic examination and it is more important to look for any other evidence of ocular involvement such as lid lag, Lagophthalmos and lid retraction .

Ocular myasthenia usually tends to present with involvement of the superior rectus and LPS muscle rather than with a involvement of Inferior rectus . There may also be a variability of the symptoms of diplopia .

Isolated inferior rectus palsy due to a midbrain lesion may result from involvement of the inferior rectus subnucleus of the oculomotor nuclear complex. At the most rostral part of the midbrain, the dorsal cell column innervating the inferior rectus is located in relative isolation. Therefore, a lesion selectively involving this area may cause isolated inferior rectus palsy.

However patients have midbrain infarction are more likely to be elderly patients with a definitive history of ischaemic risk factors.