parese n.iii oculomotorius in ophthalmology

parese n oculomotorius

1. FARADHILLAH A. SURYADI SUBDIVISI NEURO-OFTALMOLOGI THIRD CRANIAL NERVE PALSY

2. ANATOMY

3. ANATOMY

4. ETIOLOGY Most isolated unilateral CN III palsies result from (presumed) microvascular injury in the subarachnoid space or cavernous sinus. Less common causes include aneurysmal compression, tumor, inflammation (eg, sarcoidosis), vasculitis, infection (eg, meningitis), infiltration (eg, lymphoma, carcinoma), and trauma . Genetic oculomotor nerve palsy could be congenital due to hereditary cause. The mode of transmission could be either autosomal dominant or recessive.

5. CLINICAL CLASSIFICATION

6. VS N. VI (M. Rectus Lateralis) VS N. IV (M. Superior Obliq)

7. VS N. VI (M. Rectus Lateralis) VS N. IV (M. Superior Obliq)

8. CLINICAL FEATURES Complete paralysis results in limited adduction, elevation, and depression of the eye, causing exotropia and often hypotropia . The Pupil may or may not Involved

9. Partial cranial nerve (CN) III palsy. This 62- year- old woman reported experiencing “the worst headache of my life.” A, Examination revealed complete ptosis on the right; a nonreactive, dilated pupil; and severely limited extraocular movement except for abduction. B, Lateral view of a ce re bral angiogram demonstrates a posterior communicating artery aneurysm (arrow). (Part A courtesy of Steven A. Newman, MD; part B courtesy of Leo Hochhauser, MD.)

10. Clinical Features These findings are expected because the remaining unopposed muscles are the lateral rectus (abductor) and the superior oblique (abductor and depressor) , except when the cause of the paralysis involves the nerves supplying these muscles as well. Partial paralysis CN III are more common; they Present with variable limitation of supraduction, infraduction , adduction, and variable ptosis with or without pupillary dysfunction .

11. Clinical Features Adults with an acute acquired third nerve palsy usually complain of the sudden onset of binocular horizontal, vertical, or oblique diplopia and a droopy eyelid. Infrequently, the patient is aware of an enlarged pupil. Patients with chronic third nerve palsies (especially with primary aberrant regeneration ) maybe asymptomatic Pain accompanying the onset of third nerve palsy is common, except in midbrain lesions, and is not useful to distinguish among etiologies .

12. Clinical Features Pupil-involving third cranial nerve palsy Pupillary dysfunction with CN III palsy results from loss of parasympathetic input and produces a mid-dilated pupil that responds poorly to light. Patients may present with variable dysfunction of the levator palpebrae or extraocular muscles .

13. Clinical Features A patient who presents only with efferent pupillary dysfunction but exhibits normal eyelid and extraocular muscle function almost always has a benign disorder. Pupillary dysfunction, or a progressive loss of function, does not always indicate the presence o f an aneurysm or other serious problem. The vasculopathic form of a CN III palsy may produce some efferent pupillary defect in up to 20% of cases, although the pupillary involvement is generally mild (typically ≤1 mm anisocoria). Elevated fasting blood glucose, HbA1C, serum lipid levels, or blood pressure indicate an increased probability that microvascular ischemia is the cause of the CN III palsy; however, patients with these risk factors may also harbor aneurysms. Thus, pupillary involvement should prompt neuroimaging in search of an aneurysm.

14. THIRD NERVE PALSY on Children In children, third nerve palsy can be congenital (more appropriately termed dysinnervation ) or can be caused by conditions such as trauma, inflammation, or viral infection, can also occur (infrequently) as a result of a neoplastic lesion . With congenital third nerve palsies may not complain of diplopia because they ignore or suppress the second image or because they have superimposed amblyopia; often they are brought to medical attention by their parents, who have noticed ptosis or strabismus.

15. DIFFERENT DIAGNOSIS As with all motility disturbances, ocular Myastenia gra­vis can mimic virtually all components of a CN III palsy except pupillary involvement . Graves disease can affect multiple extraocular muscles, but in Graves disease the eyes are much more likely to be esotropic , rather than exotropic .

16. DIAGNOSTIC WORK UP Funduscopy Examination Laboratory Testing : Microvascular : HbA1C, Fasting Glucose Inflammatory : ANA, CMP Imaging Brain : CT / MRI Intracranial vasculature : CTA, MRA, DSA

17. MANAGEMENT Emergent cerebrovascular imaging ( eg , catheter angiography, magnetic resonance angiography [MRA], or computed tomography angiography [CTA], depending on clinical scenario and neuroradiologic consultation should be undertaken.

18. MANAGEMENT One can give the patient multivitamin injections and tablets and treat the cause like diabetes or hypertension. The surgical management of a complete III nerve paralysis, A very good method to treat this condition is to do a tenotomy of the lateral rectus and the superior oblique combined with a transposition of the vertical recti muscles to the insertion of the medial rectus muscle. If the patient has a partial palsy with slight medial rectus movement one can perform a maximal recession of the lateral rectus muscle (at least 12 mm) and resection of the medial rectus (at least 7 mm) with upward transposition of the tendons in case of an associated hypotropia.

19. MANAGEMENT The patient should be evaluated at each follow up with a complete squint work- up, diplopia charting and Hess-charting. Ischemic neuropathies usually resolve in 6 weeks to 12 weeks and can be treated conservatively Mono neuropathies with aneurysmal compressions or other compressive lesions require neurosurgical referral and intervention.

20. TERIMA KASIH