acquired oculomotor nerve palsy

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Acquired Oculomotor Nerve Palsy

From EyeWiki

Acqui red ocu lom otor ne rve pal sy(OMP) is an ocula r patho logy resulting from damage to thi rd cranial nerve. It can presents in di fferent ways causing somati c extraocula r muscledysfunction (superior, inferior, and medial recti; inferior oblique; and levator palpebrae superioris) and autonomic (pupillary sphincter and ciliary) muscles. (1)

Contents

1 Disease Entity

1.1 Disease

1.2 Etiology1.3 Risk Factors

1.4 General Pathology

1.5 Pathophysiology

1.6 A.Lesions at Oculomotor Nucleus (Midba in)

1.7 B.Lesions at Oculomotor Nerve Fascicles (Leaving the 3rd nerve nucleus)

1.8 C.Lesions in the Subarachnoid space

1.9 D.Lesions within the Cavernous Sinus and Superior Orbital Fissure

1.10 E.Lesions within the Orbit

1.11 Primary prevention

2 Diagnosis

2.1 History

2.2

2.3 Physical examination

2.4 Signs

2.5 Symptoms

2.6Clinical diagnos

2.7 Diagnostic procedures

2.8 Laboratory test

2.9 Differential diagnosis

3 Management

4 References

Disease Entity3rd nerve pal sy, partial: 378.51, 3rd nerve pal sy, total: 378.52

Disease

Clinical findings of acquired third nerve palsy depend on the affected area of the oculomo tor nerve track. It can be divided into pa rtial or complete palsy. Comple te 3rd nerve palpresents with compl ete ptosis, with the eye positioned downward and outward and unable to adduct, infraduct, or supraduct, and di lated pupil with sluggish reaction. (1) Partial 3 rd

nerve palsy are more common, and presents with a variable duction limitation of the affected extraocular muscles and with variable degree of ptosis and/or pupil dysfunction. (1)

Etiology

There are m any etio logi es for oculomotor palsy: vasculopath ic process, trauma, compression (e.g. aneurysm) and/or infi ltrative (e.g. leukemia), toxic (e.g. chemotherapy).

Risk Factors

Diabetes mell itus, Hypertension, Vasculi tis, Trauma, Infections, Tumors

General Pathology

The mani festations depend on the affected area of 3rd nerve track. In some cases, the precise site of the l esion is clear, whereas in others, the l ocation of the l esion is speculati ve.

Pathophysiology

To understand the pa thophysiology of the oculomo tor nerve palsy it is essential to know its track. The fol lowing fl owchart presents CN 3 trail with designated description of cli nicalmanifestations
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A.Lesions at Oculomotor Nucleus (Midbain)

Usuall y produce bil ateral defects. This is explained by the anatomy of the nucleus. It is divided in subnucle i according to the enervated area. Each superior recti (SR) are enervateby contralateral CN III subnucleus for this reason a nuclear CN III palsy would produce paralysis of the contrala teral SR. Both l evator palpebrae superioris are inne rvated by the one

subnuclei (central caudal nucleaus) for this reason a nuclear affectation would produce bilateral ptosis. Patients with damage to the oculomotor nuclear complex need not have

ipsilateral pupillary dilation, but when involved, it indicates dorsal rostral damage. (2) Mostly caused by ischemia, usually from embolic or thrombotic occlusion of small, dorsalperforating branches of the mesencephalic portion of the basila r artery. (2)

B.Lesions at Oculomotor Nerve Fascicles (Leaving the 3rd nerve nucleus)

Lesions at this level can produce complete or incomplete palsies. The majority of the time it cannot be differentiated from lesion outside of the midbrain. When the lesion is

adjacent to CN III nucleus (midbrain) it can produce several manifestations that have been described according to other neurological manifestations. Lesion at the superior cerebe
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peduncle(Nothnagels Syndrome)presents ipsilateral 3 rd nerve palsy and cerebel lar ataxia . Lesions at the Red Nucleus (Benedikt's Syndrome) are characterized by ipsilateral 3r

nerve palsy and contralateral involuntary movement. Lesion at the crebellar peduncle (Webers Syndrome)produces ipsilateral 3rd nerve palsy and contralateral hemiplegia. It isimpo rtant to remember that lesions can present combi nation of these findings dependi ng on the degree of the i nsult. In addition, although it i s classic that CN III separates in supeand i nferior ramii at the superior orbital fissure, sometim es lesions at the fascicles can produce isolated dysfunction of e ither the superior and inferio r division. (2) The most commo

causes are ischemic, hemorrhagic, compressive, in filtrative, traumati c, and rarely, infil trative and dem yelini zating process.

C.Lesions in the Subarachnoid space

Thi s space i s defined as the area traveled by the ocul omotor nerve between the ventral surfaces of the m idbrain to the en trance of the cavernous sinus, also known as the

interpeduncular fossa. Oculomo tor nerve damage i n this area can produce varied presentations. CN III palsy with fixed dilated pupil, it is important to recall that pupillary fibersoccupy a periphe ral locati on and recei ve more coll ateral bl ood supply that the m ain trunk of the nerve. (2) This is why they are susceptibl e to compression (e.g. aneurysm). The mo

common known etiol ogy is a posterior commun icating artery aneurysm. Thi s is a medi cal emergency. CN III palsy without pupil involv ement, as mentioned above pupillary fibers

occupy a periphe ral locati on and recei ve more coll ateral bl ood supply that the m ain trunk of the nerve. (2) For this reason are less susceptibl e to ischemia.. T his is why in most of t

cases patients have diabetes melli tus, systemic hypertension, atherosclerosis and in some cases migraine. Nevertheless, compressive masses or aneurysm can also cause it. On thecourse to the cavernous sinus the CN III rest on the edge of the ten torium cerebell i. The edge o f the uncal portion overli es the tentorium for this reason in the setting of in creased

intracranial pressure this brain section can herniate producing displacement of the midbrain compressing the ipsilateral oculomotor nerve. This causes ipsilateral ophthalmoplegia

and mydriasis. The most common cause of uncal herni ation i s intracrania l hemorrhages.

D.Lesions within the Cavernous Sinus and Superior Orbital Fissure

Lesion at these zones can produce i solated CN III palsy, but it is most commonly associated with other cranial nerves dysfunctions. Differentiating between lesions at the cavernous

sinus versus the superior orbital fi ssure can be chal lengi ng and sometimes the l iteratures describe it as sphenocavernous syndrome. It presents as paresis of oculomotor, trochlear anabducens nerves with associated m axill ary division of trigemi nal nerve, producing pai n. Thi s can be caused by primary (direct invasion) or secondary (intracranial/in traorbital le sion

compressing these areas) lesions. Most common causes are tumor (e.g. m ening iomas) There i s another described pathology within the cavernous sinus and superior orbital fissure t

presents with pai nful ophthalm opleg ia known as Tol osa Hunt Syndrome. It is described as an idi opathic granul omatous inflam mation . Thi s is a diagnosis of exclusion, thereforetumors, metastasis or aneurysm must be ruled out with neuroimaging. Although tumor are the most common causes of lesions at this zone, vascular processes can also produce

damages to the structures present i n i t. Cavernous sinus thrombosis, carotid cavernous fistulas, syphili s, vasculitis, and/or au toimmune connective tissue d iseases (e.g. systemic lupu

erythematosus) can produce pai nful ophthalm olegi as typical of cavernous sinus syndrome.(2)

E.Lesions within the Orbit

Lesions within the orbit are associated with visual loss, ophthal mopl eagia and proptosis. 3rd nerve ophthalm opleg ia can be associated with trochlear and abducence nerves palsie

It is important to remember that at the orbit the ocul omotor nerve divi des into superior and inferior divi sion. T his can cause partial oculom otor nerve palsies. Most common

etiol ogies: trauma, masses, inflammati on, and/o r infil trative processes.

Primary prevention

Although there are many risk factors, some of them can be control led to m ini mized the risk of acquiri ng oculomotor nerve palsy. It i s encouraged to m ain taing bl ood pressure and

glycemi c control which are the most common causes of vasculopathi c third nerve palsy.

DiagnosisAcqui red ocu lom otor ne rve pal sy is a clin ical diagnosis.

History

The most common ocular manifestations are dipl opia and ptosis. In addition, dependi ng on affected section of the third craneal nerve track it can also produce other neurologi cmanifestations as involuntrary movements, hemiplegia, and altered mental status.

Physical examination

Consist on complete ophthalmic exam including visual acuity, ductions and versions, levator function, pupils reaction to light and to accommodation. In addition, general physicaland/or neurological evaluation should be consider.

Signs

The presenting signs depend on the affected area of 3 rd nerve track. In some cases, the precise site of the l esion is clear, whereas in others, the l ocation of the l esion is speculati ve

can present in different ways causing somatic extraocular muscle dysfunction (superior, inferior, and m edial recti; inferior obl ique; and levator pal pebrae superioris) and autonom ic

(pupill ary sphincter and cili ary) muscles. (1)

Symptoms

Symptoms depends on the location of the lesion. The most common ocular complaint is diplopia secondary to somatic extraocular muscle dysfunction, but pain and ptosis can als

me present.

Clinical diagnos

DIagnosis is made by physical exami nation.

Diagnostic procedures

Acqui red ocu lom otor ne rve pal sy can be secondary to many e tiol ogi es. Neverthel ess, neuroimagi ng i s usual ly done special ly i f in tracranea l patho logy is suspected. In a conscious

patien t presenting with ophthal moplegia, ptosis and mydriasis a compressive eti ology, as an intracraneal aneurysm, must be ruled out. If an i ntracraneal aneurysm is suspected a

computed tomography angiography (CTA) and/or magnetic resonance imaging (MRI) must be done, with a 90% sensitivity in aneurysms of 3mm or greater in diameter, although tgold standard is the di gital substraction angiog raphy (DSA).

Laboratory test

If a patien t presents with compl ete oculom otor nerve palsy without pupil invol vement it i s most likely to be rel ated to ischemic process, but compression and infl ammati on must beconsidered. Evaluation and management wil l vary according to patients systemic i llnesses, age, and associated symptoms. Nevertheless, basic workup must be done. Th is includes

the fol lowing: vital signs (e.g. blood pressure), complete bl ood count (CBC), sedim entation rate (ESR), comprehensive metabol ic panel (CMP), central nervous system im aging (MR

or CT) can also be used to ruled out acute intracranial pathology, especially if ophthalmoplegia is associated with pain. (2)
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Differential diagnosis

Myasthenia Gravis, Thyroid associated orbitopathy, Internuclear ophthalmoplegi a, Chronic progressive external ophthalm oplegi a, Orbital pseudotumor, Giant cell arteritis

ManagementAcqui red ocu lom otor ne rve pal sy evalua tion depends on signs and symptoms, patien ts age and systemi c diseases. Management depends on the presented scenarios. In a conscio

patien t presenting with ophthal moplegia, ptosis and mydriasis a compressive eti ology, as an intracraneal anurysm, must be ruled out. In the o ther hand i f a patien t presents withcomplete oculomotor nerve palsy without pupil involvement it is most likely to be related to ischemic process, but compression and inflammation must be considered. The majority

comple te or incompl ete CN III palsy without pupi l in volvemen t are secondary ischemic process. These patients observe an im provement after the first 4 weeks with full resoluti on in

12 weeks of the i nsult. (9) Those patients presenting with that are l eft with a residual deficit can submitted to strabismus surgery after 6 of stability to maximi ze the possibi lity o fspontaneous resolution and surgical outcome. In these cases the mai n goal of strabismus surgery is to provide al ignment in prim ary and reading position.

References(1) BCSC Neurophthalmology : Chapter 8 The patient with diplopia. P.228-229 2010-2011. (2) Miller, N and Newman, N. Clinical neuro-ophthalmology 5th edition. P. 1194-1223

Kline, Lanni ng B. Neuro-Opthalmol ogy. 6th edi tion. P. 95-105 (4) Kaiser, Peter. MD., Friedman, Neil. M D., Pineda, Roberto. MD. Thi rd cranial nerve pal sy. The M assachusetts eye

and ear infirmary Illustrated manual of Ophthalmology. 2nd edition. P. 39-41 (5) Bhatt, VR. Naqi, M. Bartaula R., Murukutla S., Misra, S. Popalzai, M., Paramanathan, K. Dai, Q. Tcell acute lymphoblastic leukaemia presemting with sudden onset right oculomotor nerve palsy with normal neuroradiography and cerebrospinal fluid. BMJ Case Rep. 2012 Mar

27;2012. (6) Appenzel ler S, Veil leux, M. Clarke, A. Lupus. Thi rd cranial nerve pal sy or pseudo 3rd nerve pal sy of myasthenia gravis? A challeng ing d iagnosis in systemic l upus

erythematosus. 2009 Lupus. Aug;18(9):836-40. (7) Chaudhary,N. et al Imaging of Intracranial Aneurysms Causing Isolated Th ird Nerve Palsy. J. Neuro-Ophthalmol 2009;29:238-24

(8) Trobe,J. Searching for Brain Aneurism in T hird Cranial Nerve Palsy. J Neuro-Ophthalmol vol. 29,No.3,2009 pg.171 -3 (9) Capo, H., M.D., Warren, F., M.D., Kupersmith, M . , M.DEvolution of Oculomotor Nerve Palsies. Journal of Clincal Neuro-ophathalmology (12)1:21-25, 1992.

Original artic le contributed by: Betsy Colon-Acevedo, M D

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