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Table of Contents    
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1689-1691

Pituitary Apoplexy Presenting as Isolated Unilateral Third Nerve Palsy

Department of Neurosurgery, Goverment Medical College and Hospital, Chandigarh, India

Date of Submission31-Jul-2019
Date of Decision04-Nov-2019
Date of Acceptance27-Sep-2020
Date of Web Publication30-Aug-2022

Correspondence Address:
Vipin K Gupta
1222, Ground Floor, GMCH Campus Sector - 32, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.355153

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How to cite this article:
Gupta VK, Mamik HK, Gupta N, Bhagat RK. Pituitary Apoplexy Presenting as Isolated Unilateral Third Nerve Palsy. Neurol India 2022;70:1689-91

How to cite this URL:
Gupta VK, Mamik HK, Gupta N, Bhagat RK. Pituitary Apoplexy Presenting as Isolated Unilateral Third Nerve Palsy. Neurol India [serial online] 2022 [cited 2022 Oct 2];70:1689-91. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1689/355153


Pituitary apoplexy is a syndrome of sudden onset headache, visual deficit, ophthalmoplegia, and altered mental status caused by an expanding mass within the sella turcica due to hemorrhage or infarction of the pituitary gland.[1] Isolated oculomotor nerve palsy as a sign of pituitary apoplexy is a rare phenomenon.[2]

  Case 1: 40-Year-Old Male with Drooping of the Right Eyelid and Double Vision for 10 Days Top

Right eye showed ptosis, mydriasis, and outward gaze palsy with no visual loss suggestive of sudden onset isolated right third nerve palsy. Contrast-enhanced magnetic resonance imaging (CE-MRI) of the brain was suggestive of a sellar lesion with areas of hemorrhage compressing the right cavernous sinus and cavernous part of the right internal carotid artery (ICA). A possibility of pituitary adenoma with apoplexy was considered. Endoscopic Endonasal Trans-sphenoidal excision of the pituitary tumor was performed and a greyish-white tumor with hemorrhagic and necrotic contents was removed. Histopathological examination (HPE) was suggestive of pituitary adenoma with apoplexy. A month later, the ptosis and diplopia had resolved and mydriasis partly recovered. Postoperative CE-MRI showed no residual tumor. Oculomotor palsy recovered almost completely in 5 months [Figure 1].
Figure 1: (a). Preoperative image showing right eyelid ptosis. (b). Preoperative image showing mydriasis in the right eye. (c). Preoperative MRI showing posterolateral expansion of pituitary on the right with subsequent oculomotor nerve compression. (d). Histopathology showing pituitary apoplexy. (e). Postoperative image showing complete resolution of ptosis and near complete resolution of mydriasis. (f). CT image showing erosion of posterior clinoid process (right)

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  Case 2: 60-Year-Old Female with Headache for One Month and Sudden Onset Drooping of Right Eyelid with No Change in Vision Top

Right-sided ptosis with mydriasis was seen. MRI Brain showed a pituitary macroadenoma sized 34 × 28 × 23 mm encasing the right ICA with cystic degeneration. Endonasal hypophysectomy with lumbar drain placement was done and a soft suckable tumor with hemorrhagic contents was removed. Complete resolution of ptosis and slight mydriasis with no visual disturbances was seen at 6 months [Figure 2].
Figure 2: (a). Preoperative image showing right eyelid ptosis. (b). Postoperative image showing resolution of ptosis and mydriasis. (c). MRI images showing the expansion in pituitary and subsequent compression and resolution thereof. (d). Histopathological image suggestive of pituitary apoplexy. (e). Postoperative slit lamp image showing resolution of mydriasis and ptosis

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About 40% of patients with pituitary apoplexy have cranial nerve (CN) palsies.[3] In a study, Hage et al.[4] found CN VI palsy was the most frequent (78%) and 1 out of 27 patients examined had isolated oculomotor palsy. Oculomotor palsy without Optic nerve involvement is very rarely the presenting sign of a pituitary adenoma. Ophthalmoplegia occurs late in the clinical course[5] and may occur slowly due to mechanical compression or rapidly, secondary to pituitary apoplexy. Cerebral aneurysm (posterior communicating artery aneurysm) is the commonest differential diagnosis when the Oculomotor palsy is preceded by a severe acute headache.[6]

Kobayashi et al. described isolated oculomotor palsy in two patients due to mass effect.[5] Posterior clinoid process may erode with macroadenomas or sudden expansion due to hemorrhage. Oculomotor nerve lies in the same plane as the pituitary gland. Latero-posterior protrusion of tumor may thus cause oculomotor palsy due to compression of the nerve as it enters the cavernous sinus in the oculomotor trigone. CN III passes through this triangle through a region of dural weakness.[5] The CN IV and CN VI are less affected as they run through the tentorial fold, and inferior to the clinoid process, thus avoiding impingement.

Chronic compression by the tumor gradually erodes the clinoid process. In the event of hemorrhage, maximum pressure is transmitted to this already weakened region thus causing ipsilateral oculomotor nerve palsy.[5],[7] In both these cases, the pituitary tumor shows a posterolateral extension upholding the proposed mechanism of compression in the oculomotor trigone [Figure 3].
Figure 3: CT and Diagramatic representation of normal anatomy

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MRI with and without gadolinium DTPA enhancement provides excellent anatomical details. When correctly diagnosed and treated timely, the oculomotor dysfunction is largely reversible.[8]

Pituitary apoplexy is treated as a neurosurgical emergency and is addressed early. In atypical presentations, diagnosis and treatment may be grossly delayed. Both the patients discussed above were operated within a month and went on to make a full recovery suggesting the reversibility of the condition. Pituitary apoplexy may thus be kept as a differential for patients with unexplained isolated oculomotor dysfunction and early neurosurgical intervention may optimize the course of treatment and recovery [Table 1].
Table 1: Studies reporting isolated oculomotor palsy with pituitary apoplexy

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Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Raina S, Jerath V, Sharma A, Sharma R, Mistry K. Postpartum pituitary apoplexy with isolated oculomotor nerve palsy: A rare medical emergency. J Neurosci Rural Pract 2015;6:598-600.  Back to cited text no. 1
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Cho W, Joo S, Kim T, Seo B. Pituitary apoplexy presenting as isolated cranial nerve palsy with ptosis: Two case reports. J Korean Neurosurg Soc 2009;45:118-21.  Back to cited text no. 2
Nawar R, Abdelmannan D, Selman W, Arafah B. Analytic review: Pituitary tumor apoplexy: A review. J Intensive Care Med 2008;23:75-90.  Back to cited text no. 3
Hage R, Eshraghi S, Oyesiku N, Ioachimescu A, Newman N, Biousse V, et al. Third, fourth, and sixth cranial nerve palsies in pituitary apoplexy. World Neurosurg 2016;94:447-52.  Back to cited text no. 4
Kobayashi H, Kawabori M, Terasaka S, Murata J, Houkin K. A possible mechanism of isolated oculomotor nerve palsy by apoplexy of pituitary adenoma without cavernous sinus invasion: A report of two cases. Acta Neurochirurgica 2011;153:2453-6.  Back to cited text no. 5
Hata N, Inoue T, Katsuta T, Iwaki T. Ectopic pituitary adenoma in the cavernous sinus causing oculomotor nerve paresis--case report. Neurol Med Chir (Tokyo) 2003;43:399-403.  Back to cited text no. 6
Rossitch E Jr, Carrazana EJ, Black PMJ. Isolated oculomotor nerve palsy following apoplexy of a pituitary adenoma. Neurosurg Sci 1992;36:103-5.  Back to cited text no. 7
Saul RF, Hilliker JK. Third nerve palsy: The presenting sign of a pituitary adenoma in five patients and the only neurological sign in four patients. J Clin Neuroophthalmol 1985;5:185-93.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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