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| LETTER TO EDITOR |
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| Year : 2006 | Volume
: 54
| Issue : 4 | Page : 286-287 |
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Isolated nuclear oculomotor nerve palsy due to a solitary midbrain metastasis: A rare presentation
Manish Modi1, Veenu Singla2, Rohit Bhatia3, Rajashekhar Reddi1
1 Department of Neurology, PGIMER, Chandigarh, India
2 Department of Radiodiagnosis, PGIMER, Chandigarh, India
3 Department of Neurology, AIIMS, New Delhi, India
Correspondence Address:
Manish Modi
Department of Neurology, PGIMER, Chandigarh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0301-4738.27964
How to cite this article:
Modi M, Singla V, Bhatia R, Reddi R. Isolated nuclear oculomotor nerve palsy due to a solitary midbrain metastasis: A rare presentation. Indian J Ophthalmol 2006;54:286-7 |
Dear Editor,
Oculomotor nerve palsy is caused by numerous etiologies including aneurysms, ischemia, tumors, demyelination, meningitis, etc.[1],[2] The process may be localized to the brainstem, subarachnoid space, cavernous sinus or superior orbital fissure.[2] We present an uncommon case of a solitary midbrain metastasis from a primary tumor in the breast, producing isolated nuclear third nerve palsy with initial findings suggesting an infranuclear localization.
US, a 57-year-old female, presented with diplopia and drooping of her right eyelid. She had been diagnosed as a case of carcinoma breast (infiltrating ductal type), for which she underwent mastectomy, radiotherapy and six cycles of chemotherapy. She was on regular tamoxifen therapy. Three years later she developed diplopia with ptosis and outward deviation of her right eyeball, which evolved over 15-20 days. Examination revealed a complete third nerve palsy on the right side without any other neurological abnormality. She subsequently developed drooping of the opposite eyelid over the next few days. Examination at this time revealed ptosis and superior rectus weakness of the opposite eye also. Contrast enhanced cranial computerized tomography and magnetic resonance imaging revealed an isolated metastatic enhancing lesion in the central midbrain, ventral to the aqueduct, in the region of the oculomotor nucleus [Figure - 1]a and b. She was started on oral steroids with mild improvement of symptoms, but refused further management options.
Metastasis to the midbrain from lung, skin (melanoma), breast, epididymis, etc. has been reported as a rare cause of third nerve palsy.[3] The clinical manifestations have varied from an isolated weakness of individual extraocular muscles to a complete third nerve palsy alone, with or without other neurological signs like hemiparesis, incoordination, sensory disturbances and even dementia.[3] Lesions of the oculomotor nuclear complex usually differ from the lesions of the fascicles or the nerve proper due to topographic subgrouping of neurons in a rostrocaudal direction.[4] Each subnucleus is paired except for the unpaired central caudal nucleus supplying the levator palpebrae superioris muscle bilaterally.[2] The fibers to the superior rectus originate from the contralateral subnucleus after crossing within the nuclear complex. Parasympathetic fibers for pupillary contraction originate from the juxtaposed Edinger-Westphal nuclei. The nuclear and fascicular arrangement is thus speculated to control pupillary, extraocular and eyelid elevation in the rostrocaudal order.[5] Thus, rostral lesions may spare the caudal levator complex and dorsal lesions may spare the Edinger-Westphal nucleus.[2] This organization may lead to varied manifestations such as unilateral third nerve paresis, isolated rectus weakness, skew deviation and isolated unilateral or bilateral ptosis, absence of ptosis or pupillary involvement.[5] Larger lesions of the midbrain tend to present with additional neurological signs, aiding in localization. Our patient initially presented with features of a progressively increasing third nerve paresis in the absence of long tract signs, suggesting a peripheral cause. Subsequent clinical and imaging features however confirmed its central origin. This case highlights the rarity of isolated midbrain metastasis and its presentation as an isolated, slowly evolving nuclear oculomotor nerve palsy and justifies the importance of realizing the architectural organization of this nerve responsible for its varying clinical presentations.
| References | |  |
| 1. | Bennett JL, Pelak VS. Palsies of the third, fourth and sixth cranial nerves. Ophthalmol Clin North Am 2001;14:169-85.  [ PUBMED] |
| 2. | Rush JA, Younge BR. Paralysis of cranial nerves III, IV and VI. Cause and prognosis in 1,000 cases. Arch Ophthalmol 1981;99:76-9. [ PUBMED] |
| 3. | Keane JR, Zaias B, Itabashi HH. Levator-sparing oculomotor nerve palsy caused by a solitary midbrain metastasis. Arch Neurol 1984;41:210-2. [ PUBMED] |
| 4. | Bogousslavsky J. Oculomotor syndromes resulting from mesencephalic lesions in man. Rev Neurol 1989;145:546-59. [ PUBMED] |
| 5. | Saeki N, Yamura A, Sunami K. Bilateral ptosis with pupil sparing because of a discrete midbrain lesion: Magnetic resonance imaging evidence of topographic arrangement within the oculomotor nerve. J Neuroophthalmol 2000;20:130-4. |
[Figure - 1]
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