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 Table of Contents  
MEDICAL QUIZ
Year : 2020  |  Volume : 4  |  Issue : 3  |  Page : 148-149

Medical quiz: Ophthalmology pearl


1 Department of Medicine, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar
2 Department of Medicine, Hamad General Hospital, Hamad Medical Corporation; Department of Medicine, College of Medicine, Qatar University; Department of Medicine, Weill Cornell College of Medicine, Doha, Qatar
3 Department of Medicine, Hamad General Hospital, Hamad Medical Corporation; Department of Medicine, Weill Cornell College of Medicine, Doha, Qatar

Date of Submission13-Jul-2020
Date of Acceptance09-Aug-2020
Date of Web Publication21-Sep-2020

Correspondence Address:
Dr. Almurtada Ali Razok
Hamad General Hospital, P.O Box 3050, Doha
Qatar
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/LJMS.LJMS_59_20

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How to cite this article:
Razok AA, Malik RF, M. Elhassan AA, Elzouki AN, Zahid M. Medical quiz: Ophthalmology pearl. Libyan J Med Sci 2020;4:148-9

How to cite this URL:
Razok AA, Malik RF, M. Elhassan AA, Elzouki AN, Zahid M. Medical quiz: Ophthalmology pearl. Libyan J Med Sci [serial online] 2020 [cited 2020 Oct 20];4:148-9. Available from: https://www.ljmsonline.com/text.asp?2020/4/3/148/295617



A 47-year-old male with a background of obesity, diabetes mellitus Type II, and dyslipidemia presented with a 3-day history of right-sided loss of vision. It was sudden in onset, painless with no associated floaters or light flashes. There was no headache, photophobia, nausea, vomiting, seizures, and sensory or motor abnormalities. The patient reported a similar episode on the left side 1 year ago, which persisted and caused chronic decrease in visual acuity. Review of other systems was negative for weight loss, fever, scalp tenderness, jaw claudication, and arthralgia. A detailed neurologic physical examination did not reveal any sensory or motor abnormalities. Left-sided relative afferent pupillary defect with bilateral decrease in color vision was appreciated. Findings of fundoscopic examination are shown in [Figure 1]a (left eye) and [Figure 1]b (right eye). Magnetic resonance imaging (MRI) of the orbit, head, and spine with contrast revealed evidence of chronic optic neuritis on the left and acute optic neuritis on the right. There was no evidence of demyelination or diffusion restriction. HBA1C was 8.6%, total cholesterol 6 mmol/L, LDL 3.54 mmol/L, erythrocyte sedimentation rate (ESR) 14 mm/h, and C-reactive protein (CRP) 0.6 mg/L. Complete blood count and comprehensive metabolic panel were essentially normal. The patient's home medications included metformin 1000 mg twice daily and atorvastatin 20 mg once daily at bedtime.
Figure 1: (a) Fundoscopic examination of the left eye showing optic disc pallor and atrophy, in addition to attenuated blood vessels. (b) Fundoscopic examination of the right eye showing papilledema Grade II, with attenuated blood vessels

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  Question: What Is the Diagnosis That Best Fits With the Clinical Picture? Top


Discussion

The diagnosis is pseudo–Foster–Kennedy syndrome due to nonarteritic ischemic optic neuropathy (NAION). Fundoscopic examination revealed left optic disc pallor and atrophy [Figure 1]a and right optic disc swelling grade II [Figure 1]b, with attenuated blood vessels bilaterally.

Foster–Kennedy syndrome, also known as Gower–Paton–Kennedy syndrome, refers to a group of findings that are associated with raised intracranial pressure due to a space-occupying lesion situated in the anterior cranial fossa.[1] Type I of this syndrome includes a constellation of headache, ipsilateral optic atrophy, and contralateral optic disc swelling, while Type II and III include bilateral papilledema and bilateral optic atrophy, respectively.[2] The presence of these ophthalmic features in the absence of an intracranial mass is defined as pseudo–Foster–Kennedy syndrome, the most common reason for which is NAION.[3] Risk factors for nonarteritic ischemic optic neuropathy include hypertension, diabetes mellitus, dyslipidemia, and obstructive sleep apnea.[4] Pseudo–Foster–Kennedy syndrome can be distinguished from true Foster–Kennedy syndrome based on history, physical examination, fundoscopy, and brain imaging. Patients with classic type I Foster–Kennedy syndrome present with progressive unilateral visual loss in the atrophied side, with asymptomatic contralateral papilledema; however, patients with pseudo–Foster–Kennedy typically have a history of sequential loss of vision with papilledema which later progresses to optic atrophy.[5]

Acute loss of vision has many differentials depending on the acuity of presentation, presence or absence of pain, associated symptoms, and laterality. These include retinal artery occlusion, retinal vein thrombosis, optic neuritis, increased intracranial pressure, and ischemic optic neuropathy.

The negative MRI of the head and absence of headache and other symptoms of increased intracranial pressure make idiopathic and secondary intracranial hypertension unlikely. Painless loss of vision, normal motor and sensory examination, negative Uhthoff's phenomenon, and the absence of demyelinating lesions on MRI of the head and spine make multiple sclerosis and neuromyelitis optica less likely. The patient's age, gender, absence of constitutional symptoms with negative antineutrophil cytoplasmic antibody test, and normal ESR and CRP render arteritic ischemic optic neuropathy due to underlying giant cell arteritis unlikely. The progressive nature of symptoms and absence of cherry red spot on fundoscopic examination make amaurosis fugax and retinal artery occlusion less likely, respectively.

Declaration of patient consent

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

Acknowledgment

The authors would like to thank the ophthalmologist, Dr. Nour Barakat, for her contribution in this manuscript by providing the fundoscopic images and their corresponding explanation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sadun A and Agarwal M. Topical diagnosis of acquired optic nerve disorders. In: Miller N, Biousse V, Newman N, Kerrison J, editors. Walsh and Hoyt's Clinical Neuro-ophthalmology. 6th ed.., Vol. No. 1. Philadelphia: Lippincott Williams & Wilkins; 2005; p. 228-9.  Back to cited text no. 1
    
2.
Lai AT, Chiu SL, Lin IC, Sanders M. Foster Kennedy syndrome: Now and then. J Neuroophthalmol 2014;34:92-4.  Back to cited text no. 2
    
3.
Micieli JA, Al-Obthani M, Sundaram AN. Pseudo-foster Kennedy syndrome due to idiopathic intracranial hypertension. Can J Ophthalmol 2014;49:e99-102.  Back to cited text no. 3
    
4.
Mojon DS, Hedges TR 3rd, Ehrenberg B, Karam EZ, Goldblum D, Abou-Chebl A, et al. Association between sleep apnea syndrome and nonarteritic anterior ischemic optic neuropathy. Arch Ophthalmol 2002;120:601-5.  Back to cited text no. 4
    
5.
Gelwan MJ, Seidman M, Kupersmith MJ. Pseudo-pseudo-Foster Kennedy syndrome. J Clin Neuroophthalmol 1988;8:49-52.  Back to cited text no. 5
    


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