Medical Journal of Dr. D.Y. Patil Vidyapeeth

CASE REPORT
Year
: 2014  |  Volume : 7  |  Issue : 3  |  Page : 385--387

Pseudo Foster Kennedy Syndrome secondary to uncontrolled hypertension and diabetes mellitus: A case report


Kavita R Bhatnagar1, Charu Raulji2, Pooja Kumar2, Dependar Solanki2,  
1 Department of Ophthalmology, Padmashree Dr D Y Patil Medical College, Hospital and Research Centre, Dr. D Y Patil Vidyapeeth, Pimpri, Pune, India
2 Department of Ophthalmology, SBKS medical Institute and Research Center, Vadodara, Gujarat, India

Correspondence Address:
Kavita R Bhatnagar
B 4/21, Brahma Aangan, Off Salunke Road, Kondhwa, Pune - 411048
India

Abstract

Pseudo-Foster Kennedy Syndrome is described as unilateral optic disc swelling with contra lateral optic atrophy in the absence of an intracranial mass causing compression of the optic nerve. This occurs typically due to bilateral sequential optic neuritis or ischemic optic neuropathy. We describe a case of pseudo-Foster Kennedy Syndrome in a 37-year-old male with unilateral papilledema secondary to malignant hypertension and pre-existing ischemic optic neuropathy in other eye preventing transmission of raised intracranial pressure to the optic nerve. Hypertension and diabetes mellitus (DM) play a significant role in pathogenesis of ischemic optic neuropathy. There is a greater correlation in patients with small disc and little to no cupping. The disorder commonly occurs in the 40-65 yrs age group. Our case is an example of Pseudo-Foster Kennedy syndrome where papilledema in one eye was associated with uncontrolled hypertension and disc pallor in fellow eye was secondary to ischemic optic neuropathy.



How to cite this article:
Bhatnagar KR, Raulji C, Kumar P, Solanki D. Pseudo Foster Kennedy Syndrome secondary to uncontrolled hypertension and diabetes mellitus: A case report.Med J DY Patil Univ 2014;7:385-387


How to cite this URL:
Bhatnagar KR, Raulji C, Kumar P, Solanki D. Pseudo Foster Kennedy Syndrome secondary to uncontrolled hypertension and diabetes mellitus: A case report. Med J DY Patil Univ [serial online] 2014 [cited 2019 Dec 10 ];7:385-387
Available from: http://www.mjdrdypu.org/text.asp?2014/7/3/385/128999


Full Text

 Introduction



Pseudo-Foster Kennedy Syndrome is described as unilateral optic disc swelling with contralateral optic atrophy in the absence of an intracranial mass causing compression of the optic nerve. This occurs typically due to bilateral sequential optic neuritis or ischemic optic neuropathy. [1] Here we present a rare case of Pseudo-Foster Kennedy syndrome where papilledema in one eye was associated with uncontrolled hypertension and disc pallor in fellow eye was secondary to ischemic optic neuropathy.

 Case Report



A 37-year-old male presented in eye department of our hospital with complains of gradual onset painless diminution of vision associated with photopsia in right eye (OD). There were no complaints in left eye (OS). There was no past history suggestive of hypertension, diabetes, or any other major systemic illness. Patient's mother was a known case of hypertension and diabetes. On examination, best-corrected visual acuity (BCVA) was 6/60 and 6/6 in OD and OS, respectively. Intraocular pressure was 17.3 in both eyes. Pupil showed relative afferent papillary defect (RAPD) in OD. Fundus examination of OD showed the presence of disc edema while left optic nerve head did not. Mild exudation was seen next to the temporal portion of the nerve [Figure 1]a and b. Fundus Fluorescein angiography showed swollen right optic disc with hemorrhages due to current ischemic episode. Early phase of fluorescein angiogram of right eye showed poor perfusion of optic disc and dilated superficial disc capillaries. Late phase of fluorescein angiogram showed disc leakage. His blood pressure was 168/116 mmHg and random blood sugar level was 331 mg/dl. His X-ray chest, CT scan, and MRI reports were normal. Serum creatinine was 1.0 mg%. All hematological investigations including ESR and C-reactive protein were within normal range. Physician reference was done for elevated sugar levels and high blood pressure. He was subsequently started on antidiabetic and antihypertensive drugs. The patient was called for follow up after 2 months with the same medical treatment for evaluation of disc edema and status of hypertensive and diabetic retinopathy changes. On his follow up visit, his visual acuity was OD:6/60 and OS:6/6. RAPD was present in OD. Blood pressure was 170/96 mmHg. Fasting blood sugar was 326 mg%. Fundus examination revealed following findings. The right optic nerve head showed less disc edema but the optic disc pallor became evident at this time [Figure 2]a. The picture may not do justice to the superior differentiation of the pallor. Loss of the superior nerve fiber layer was noted. The left optic nerve head showed signs of acute papilledema [Figure 2]b. These findings can be described as Pseudo-Foster Kennedy Syndrome.{Figure 1}{Figure 2}

 Discussion



The appearance of unilateral optic disc swelling with contralateral optic disc atrophy has been described as the Foster Kennedy Syndrome. In "true" Foster-Kennedy Syndrome unilateral disc swelling is caused by a tumor on the inferior surface of the frontal lobe, compressing the optic nerve on one side with papilledema contralaterally. [1] In the absence of an intracranial mass these findings may be labeled as pseudo-Foster Kennedy Syndrome, typically due to bilateral sequential optic neuritis or ischemic optic neuropathy. [2],[3],[4] In Pseudo-Foster Kennedy syndrome, the diagnosis is more commonly a disease of exclusion. Normal MRI and CT imaging eliminate the existence of any intracranial lesions.

Explanations for the unilateral disc swelling in Foster Kennedy syndrome include failure of transmission of the intracranial pressure to the optic disc secondary to pressure on the vaginal sheath or closure of the vascular bed of the optic disc. [5] Our case is an example of Pseudo-Foster Kennedy Syndrome where papilledema in one eye was associated with uncontrolled hypertension and disc pallor in fellow eye was secondary to ischemic optic neuropathy.

Hypertension and diabetes mellitus (DM) play a significant role in pathogenesis of ischemic optic neuropathy which may predispose to optic nerve infarction. Another important factor is the size of cup to disc ratio. There is a greater correlation in patients with small disc and little to no cupping. The disorder commonly occurs in 40-65 yrs age group. [3] In our case, all three risk factors were present for developing ischemic optic neuropathy. Management of the patient's condition included control of hypertension and diabetes.

In our case, the patient's previous diagnosis and partial resolution of ischemic optic neuropathy created the unique ocular picture of Pseudo-Foster Kennedy Syndrome.

 Conclusion



Hypertension and DM play a significant role in pathogenesis of ischemic optic neuropathy. There is a greater correlation in patients with small disc and little to no cupping. The disorder commonly occurs in 40-65 yrs age group. Our case is an example of Pseudo-Foster Kennedy syndrome where papilledema in one eye was associated with uncontrolled hypertension and disc pallor in fellow eye was secondary to ischemic optic neuropathy.

References

1Massey EW, Schoenberg B. Foster Kennedy Syndrome. Arch Neurol 1984;41:658-9.
2Bansal S, Dabbs T, Long V. Pseudo-Foster Kennedy Syndrome due to unilateral optic nerve hypoplasia: A case report. J Med Case Reports 2008;2:86.
3Watnick RL, Trobe JD. Bilateral optic nerve compression as a mechanism for the Foster Kennedy Syndrome. Ophthalmology 1989;96:1793-8.
4Shatz N, Smith J. Non tumor causes of the Foster Kennedy syndrome. J Neurosurg 1967;27:37.
5Yildizhan A. A case of Foster Kennedy syndrome without frontal lobe or anterior cranial fossa involvement. Neurosurg Rev 1992;15:139-42.