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Year : 2010  |  Volume : 58  |  Issue : 5  |  Page : 820-821

Idiopathic intracranial hypertension with complete oculomotor palsy

Department of Neurology, Iran University of Medical Sciences, Tehran, Iran

Date of Acceptance22-Jul-2010
Date of Web Publication28-Oct-2010

Correspondence Address:
Arezoo Rezazadeh
Department of Neurology, Iran University of Medical Sciences, Tehran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.72210

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How to cite this article:
Rezazadeh A, Rohani M. Idiopathic intracranial hypertension with complete oculomotor palsy. Neurol India 2010;58:820-1

How to cite this URL:
Rezazadeh A, Rohani M. Idiopathic intracranial hypertension with complete oculomotor palsy. Neurol India [serial online] 2010 [cited 2023 Jun 7];58:820-1. Available from:


Idiopathic intracranial hypertension (IIH) is a syndrome of increased intracranial pressure without a space occupying lesion. [1] We report a unique patient with IIH presenting with complete oculomotor palsy.­­

An otherwise healthy 21-year-old woman with a past medical history of facial acne treated with isotretinoin presented with two weeks of progressive generalized headache, vomiting, blurred vision and tinnitus. There was no history of fever or past history of headache. On examination she was conscious and alert. Vital signs were normal. Blood pressure was 100/80. She had right ptosis with limitation of all right eye movements except for abduction. Right pupil was dilated and not reacting to light [Figure 1]a. Left pupil was normal. Visual acuity was one meter finger count OD and 20/80 OS. Fundus examination showed bilateral papilledema without hemorrhages. Motor and sensory systems were normal. There were no signs of meningeal irritation. Routine labs were normal. Lumbar puncture revealed an opening pressure of 400 mm H 2 O with normal composition. Imaging studies including brain computerized tomography (CT) scan, magnetic resonance imaging (MRI), MR-venography, CT angiography were normal [Figure 2]. The patient was treated with multiple lumbar punctures and acetazolamide and was discharged a few days later on acetazolamide. Follow up exams, one and six months later, showed dramatic improvement of symptoms and signs including headache, papilledema, ophthalmoplegia and dilated pupil [Figure 1]b and c. Visual acuity improved partially after one year of follow up.
Figure 1 :(a) Extraocular movement of the patient at initial presentation. Note the ptosis, adduction and depression deficit of the right eye. In addition there is pupil dilation that is not reactive to light. (b) Extraocular movement of the patient one month later. Note the partial improvement of the ptosis, adduction and depression of the right eye. (c) Extraocular movement of the patient six months later. Note the complete improvement of ptosis, adduction and depression of the right eye. In addition the light reactivity of the pupil is resolved

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Figure 2 :(a) T2 weighted axial and (b) T1 weighted sagittal MRI showing normal sized ventricles and absence of mass lesion. (c) CT angiography; Anteroposterior view of the posterior circulation; No aneurysm was detected

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The diagnostic criteria for IIH has been revised and these include: [2] (1) symptoms if present, reflect only those of increased intracranial pressure or papilledema; (2) signs attributable only to increased intracranial pressure and papilledema; (3) documented elevated intracranial pressure, during lumbar puncture measured in the lateral decubitus position; (4) normal cerebrospinal fluid composition; (5) no ventriculomegaly, mass, structural vascular lesion on neuroimaging studies. (MRI or contrast-CT for typical patients and MRI and MRV for all others); and (6) If no other cause (including medications) of intracranial hypertension is identified, the syndrome is termed Idiopathic intracranial hypertension.

In most cases the cause is unknown but can include certain drug ingestion or systemic inflammation and metabolic disease. [3] The present patient satisfied all the diagnostic criteria of IIH. Sixth nerve palsy is reported to occur in 10-40% of patient in most series of IIH, [4] which is a nonlocalizing sign of increased intracranial pressure and can be unilateral or bilateral. [2] There has been only one case report of fourth nerve palsy being associated with IIH. [5] Oculomotor palsy is an uncommon association seen in IIH, [2],[3],[4],[6],[7] in which all has been attributed to raised intracranial pressure. Pupillary fibers were spared in all the reported cases. However, the present patient is the first one in whom the pupil was affected too. This finding led us to investigate for secondary causes. The results were all normal so we concluded that third nerve palsy, involving pupil fibers, could be a nonlocalizing sign of IIH, although secondary causes exclusion is recommended.

 » References Top

1.Friedman DI. Psuedotumor cerebri. Neurol Clin 2004;22:99-131.  Back to cited text no. 1
2.Chansoria M, Agrawal A, Ganghoriya P, Raghu Raman B. Psedotumor cerebri with transient oculomotor palsy. Indian J Pediatr 2005;72:1047-8.   Back to cited text no. 2
3.Thapa R. Transient bilateral oculomotor palsy in psuedotumor cerebri. J Child Neurol 2008;23:580-1.   Back to cited text no. 3
4.McCammon A, Kaufman HH, Sears ES. Transient oculomotor paralysis in psuedotumor cerebri. Neurology 1981;31:182-4.   Back to cited text no. 4
5.Lee AG. Fouth nerve palsy in psuedotumor cerebri. Strabismus 1995;3:57-9.   Back to cited text no. 5
6.Landan I, Policherla H. Complete external ophthalmoplegia in a case of psuedotumor cerebri. Headache 1987;27:573-4.   Back to cited text no. 6
7.Bruce BB, Newman NJ, Biousse V. Ophthalmoparesis in idiopathic intracranial hypertension. Am J Ophthalmol 2006;142:878-80.  Back to cited text no. 7


  [Figure 1], [Figure 2]

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