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1 Disease Entity 1.1 1.2 1.3 1.4 1.5 1.6 Disease Etiology Risk Factors General Pathology Pathophysiology A.Lesions at Oculomotor Nucleus (Midbain)
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 2.4 2.5 2.6 2.7 Physical examination Signs Symptoms Clinical diagnos Diagnostic procedures
Disease Entity
3rd nerve palsy, partial: 378.51, 3rd nerve palsy, total: 378.52
Disease
Clinical findings of acquired third nerve palsy depend on the affected area of the oculomotor nerve track. It can be divided into partial or complete palsy. Complete 3rd nerve palsy presents with complete ptosis, with the eye positioned downward and outward and unable to adduct, infraduct, or supraduct, and dilated pupil with sluggish reaction. (1) Partial 3rd 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 many etiologies for oculomotor palsy: vasculopathic process, trauma, compression (e.g. aneurysm) and/or infiltrative (e.g. leukemia), toxic (e.g. chemotherapy).
Risk Factors
Diabetes mellitus, Hypertension, Vasculitis, Trauma, Infections, Tumors
General Pathology
The manifestations depend on the affected area of 3rd nerve track. In some cases, the precise site of the lesion is clear, whereas in others, the location of the lesion is speculative. (2
Pathophysiology
To understand the pathophysiology of the oculomotor nerve palsy it is essential to know its track. The following flowchart presents CN 3 trail with designated description of clinical manifestations
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peduncle(Nothnagels Syndrome) presents ipsilateral 3rd nerve palsy and cerebellar ataxia. Lesions at the Red Nucleus (Benedikt's Syndrome) are characterized by ipsilateral 3rd nerve palsy and contralateral involuntary movement. Lesion at the crebellar peduncle (Webers Syndrome) produces ipsilateral 3rd nerve palsy and contralateral hemiplegia. It is important to remember that lesions can present combination of these findings depending on the degree of the insult. In addition, although it is classic that CN III separates in superior and inferior ramii at the superior orbital fissure, sometimes lesions at the fascicles can produce isolated dysfunction of either the superior and inferior division. (2) The most common causes are ischemic, hemorrhagic, compressive, infiltrative, traumatic, and rarely, infiltrative and demyelinizating process.
Primary prevention
Although there are many risk factors, some of them can be controlled to minimized the risk of acquiring oculomotor nerve palsy. It is encouraged to maintaing blood pressure and glycemic control which are the most common causes of vasculopathic third nerve palsy.
Diagnosis
Acquired oculomotor nerve palsy is a clinical diagnosis.
History
The most common ocular manifestations are diplopia and ptosis. In addition, depending on affected section of the third craneal nerve track it can also produce other neurologic manifestations 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 physical and/or neurological evaluation should be consider.
Signs
The presenting signs depend on the affected area of 3rd nerve track. In some cases, the precise site of the lesion is clear, whereas in others, the location of the lesion is speculative. It can present in different ways causing somatic extraocular muscle dysfunction (superior, inferior, and medial recti; inferior oblique; and levator palpebrae superioris) and autonomic (pupillary sphincter and ciliary) 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 also me present.
Clinical diagnos
DIagnosis is made by physical examination.
Diagnostic procedures
Acquired oculomotor nerve palsy can be secondary to many etiologies. Nevertheless, neuroimaging is usually done specially if intracraneal pathology is suspected. In a conscious patient presenting with ophthalmoplegia, ptosis and mydriasis a compressive etiology, as an intracraneal aneurysm, must be ruled out. If an intracraneal 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 the gold standard is the digital substraction angiography (DSA).
Laboratory test
If a patient presents with complete oculomotor nerve palsy without pupil involvement it is most likely to be related to ischemic process, but compression and inflammation must be considered. Evaluation and management will vary according to patients systemic illnesses, age, and associated symptoms. Nevertheless, basic workup must be done. This includes the following: vital signs (e.g. blood pressure), complete blood count (CBC), sedimentation rate (ESR), comprehensive metabolic panel (CMP), central nervous system imaging (MRI 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 ophthalmoplegia, Chronic progressive external ophthalmoplegia, Orbital pseudotumor, Giant cell arteritis
Management
Acquired oculomotor nerve palsy evaluation depends on signs and symptoms, patients age and systemic diseases. Management depends on the presented scenarios. In a conscious patient presenting with ophthalmoplegia, ptosis and mydriasis a compressive etiology, as an intracraneal anurysm, must be ruled out. In the other hand if a patient presents with complete 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 of complete or incomplete CN III palsy without pupil involvement are secondary ischemic process. These patients observe an improvement after the first 4 weeks with full resolution in 12 weeks of the insult. (9) Those patients presenting with that are left with a residual deficit can submitted to strabismus surgery after 6 of stability to maximize the possibility of spontaneous resolution and surgical outcome. In these cases the main goal of strabismus surgery is to provide alignment in primary 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 (3) Kline, Lanning B. Neuro-Opthalmology. 6th edition. P. 95-105 (4) Kaiser, Peter. MD., Friedman, Neil. MD., Pineda, Roberto. MD. Third cranial nerve palsy. The Massachusetts 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. T cell 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) Appenzeller S, Veilleux, M. Clarke, A. Lupus. Third cranial nerve palsy or pseudo 3rd nerve palsy of myasthenia gravis? A challenging diagnosis in systemic lupus erythematosus. 2009 Lupus. Aug;18(9):836-40. (7) Chaudhary,N. et al Imaging of Intracranial Aneurysms Causing Isolated Third Nerve Palsy. J. Neuro-Ophthalmol 2009;29:238-244 (8) Trobe,J. Searching for Brain Aneurism in Third 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.D. Evolution of Oculomotor Nerve Palsies. Journal of Clincal Neuro-ophathalmology (12)1:21-25, 1992.
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