Oculomotor nerve palsy
| Oculomotor nerve palsy | |
|---|---|
| Specialty | Ophthalmology, neurology  |
Oculomotor nerve palsy or third 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 his or her eye normally. In addition, the nerve also supplies the upper eyelid muscle (levator palpebrae superioris) and 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).
It is also known as "oculomotor neuropathy".[1]
Eye position
A complete oculomotor nerve palsy will result in a characteristic down and out position in the affected eye. The eye will be displaced outward and displaced downward; 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).
It should be borne in mind, however, that 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, 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 lid ptosis and mydriasis (a "blown" pupil) as a result of parasympathetic fiber compression before the "down and out" position is seen.
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
- Vascular disorders such as diabetes, heart disease, atherosclerosis and aneurysm, particularly of the posterior communicating artery
- Space occupying lesions or tumours, both malignant and non-malignant
- Inflammation and infection
- Trauma
- Demyelinating disease (multiple sclerosis)
- Autoimmune disorders such as myasthenia gravis
- Post-operatively as a complication of neurosurgery
- Cavernous sinus thrombosis
Ischemic stroke selectively affects somatic fibers over parasympathetic fibers, while traumatic stroke affects both types more equally. Therefore, while almost all forms cause ptosis and impaired movement of the eye, pupillary abnormalities are more commonly associated with trauma than with ischemia.
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 edge fibers which control the pupillomotor fibers, which control the pupil.[3]
References
- ^ 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.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Goldstein, JE (1960). "Diabetic ophthalmopegia with special reference to the pupil". Arch Ophthalmol. 64: 592.
- ^ Dyck; Thomas (1999). Diabetic Neuropathy. pp. 458–459.