Oculomotor nerve palsy

Oculomotor nerve palsy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Thus, damage to this nerve will result in the affected individual being unable to move their eye normally. In addition, the nerve also supplies the upper eyelid muscle (levator palpebrae superioris) and It is accompanied by parasympathetic fibers innervating the muscles responsible for pupil constriction (sphincter pupillae) . The limitations of eye movements resulting from the condition are generally so severe that the affected individual is unable to maintain normal alignment of their eyes when looking straight ahead, leading to strabismus and, as a consequence, double vision (diplopia).

Oculomotor nerve palsy
Other namesThird nerve palsy
Eye nerves diagram
SpecialtyOphthalmology, neurology 

It is also known as "oculomotor neuropathy".[1]

Presentation

A complete oculomotor nerve palsy will result in a characteristic down and out position in the affected eye. The eye will be displaced outward "exotropia" and displaced downward "hypotropia"; outward because the lateral rectus (innervated by the sixth cranial nerve) maintains muscle tone in comparison to the paralyzed medial rectus. The eye will be displaced downward, because the superior oblique (innervated by the fourth cranial or trochlear nerve), is unantagonized by the paralyzed superior rectus, inferior rectus and inferior oblique. The affected individual will also have a ptosis, or drooping of the eyelid, and mydriasis (pupil dilation).

Cause

Oculomotor palsy can arise as a result of a number of different conditions. Non traumatic pupil-sparing oculomotor nerve palsies are often referred to as a 'medical third' with those affecting the pupil being known as a 'surgical third'.

Congenital oculomotor palsy

The origins of the vast majority of congenital oculomotor palsies are unknown, or idiopathic to use the medical term. There is some evidence of a familial tendency to the condition, particularly to a partial palsy involving the superior division of the nerve with an autosomal recessive inheritance. The condition can also result from aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve. It can also occur as a consequence of severe birth trauma.

Acquired oculomotor palsy
  1. Vascular disorders such as diabetes, heart disease, atherosclerosis and aneurysm, particularly of the posterior communicating artery
  2. Space occupying lesions or tumours, both malignant and non-malignant
  3. Inflammation and infection
  4. Trauma
  5. Demyelinating disease (multiple sclerosis)
  6. Autoimmune disorders such as myasthenia gravis
  7. Post-operatively as a complication of neurosurgery
  8. Cavernous sinus thrombosis

Ischemic stroke selectively affects somatic fibers over parasympathetic fibers, while traumatic stroke affects both types more equally. Ischemic stroke affects vasoneurium which starts to supply the nerve from outside to inside. As the somatic fibers are located inner part of the nerve, these fibres are affected more in the setting of ischemia. A similar mechanism is also accurate for diabetes. Therefore, while almost all forms ('medical third' and 'surgical third') cause ptosis and impaired movement of the eye, pupillary abnormalities are more commonly associated with trauma and the 'surgical third' than with ischemia, ie the 'medical third'. To further clarify, classically a posterior communicating artery aneurysm will cause compression of the entire third nerve and so prevent ANY nerve signal conduction thus affecting the somatic system and also the autonomic. The compression of the external autonomic fibres renders the pupil non reactive and thus leads to the surgical third nerve palsy.

Oculomotor palsy can be of acute onset over hours with symptoms of headache when associated with diabetes mellitus. Diabetic neuropathy of the oculomotor nerve in a majority of cases does not affect the pupil.[2] The sparing of the pupil is thought to be associated with the microfasciculation of the fibers which control the pupillomotor function located on the outmost aspect of the occulomotor nerve fibres; these fibres are spared because they are outermost and so less prone to ischaemic damage than the innermost fibres.[3]


Mechanism

The branched structure of the oculomotor nerve means that damage sustained at different points along its pathway, or damage caused in different ways (compression versus loss of blood supply vs neuropathy, for example), will result in different muscle groups or, indeed, different individual muscles being affected, thus producing different presentation patterns.

Compressive oculomotor nerve damage could result in compression of the parasympathetic fibers before any disruption of the motor fibers occurs, since the parasympathetic fibers run on the outside of the nerve. Therefore, one could have mydriasis (a "blown" pupil) as a result of parasympathetic fiber compression before lid ptosis and the "down and out" position are seen.

References
  1. Mohammad, J; Kefah, AH; Abdel, Aziz H (2008). "Oculomotor neuropathy following tetanus toxoid injection". Neurol India. 56 (2): 214–6. doi:10.4103/0028-3886.42013. PMID 18688160.
  2. Goldstein, JE (1960). "Diabetic ophthalmopegia with special reference to the pupil". Arch Ophthalmol. 64: 592. doi:10.1001/archopht.1960.01840010594018.
  3. Dyck; Thomas (1999). Diabetic Neuropathy. pp. 458–459.
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