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   Table of Contents      
Year : 1973  |  Volume : 21  |  Issue : 1  |  Page : 32-33

Foster Kennedy syndrome

Department of Ophthalmology, Medical College, Jabalpur, India

Correspondence Address:
Prabha Bhura
Department of Ophthalmology, Medical College, Jabalpur
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Source of Support: None, Conflict of Interest: None

PMID: 4793005

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How to cite this article:
Bhura P, Mishra R K. Foster Kennedy syndrome. Indian J Ophthalmol 1973;21:32-3

How to cite this URL:
Bhura P, Mishra R K. Foster Kennedy syndrome. Indian J Ophthalmol [serial online] 1973 [cited 2020 Dec 3];21:32-3. Available from: https://www.ijo.in/text.asp?1973/21/1/32/31421

Foster Kennedy syndrome is a well known condition of uncommon occur­rence showing optic atrophy on one side with papilloedema on the other.

  Case Report Top

N.S.P., male aged 19 years came to us on 8th February 1966 with com­plaints of diminished vision right eye, complete loss of vision left eye, in­creasing prominence of left eye, head­ache, vomiting, gradual loss of hear­ing and weakness of right leg and doubtful weakness of right arm. The patient walked in by himself but most of the talking was done by the atten­dants. He gave an impression of men­tal confusion.

Examination : The right eye was found normal externally. Vision 6/9, pupillary reaction normal, fundus showed oedema of the disc 6D with the usual picture of papilloedema and constriction of temporal half of the field.

The left eye was found to be prop­tosed down and outwards exposing the entire cornea and the surrounding congested and chemotic bulbar con­junctiva. The cornea showed a small adherent leucoma, pear shaped pupil, transparent lens, complete primary optic atrophy, normal intraocular ten­sion and vision perception of light only. The left abducent nerve was paralysed.

Systemic examination revealed right upper and lower limbs to be weak. The patient had an unsteady gait with a limp on the right side. There was right facial paresis of lower motor neuron type.

The condition continued to deterio­rate. Gradually the patient became more and more disoriented and list­less. The right hemiparesis, the facial paresis and left proptosis with abdu­cent paralysis became more and more marked. The vision in the right eye continued to deteriorate.

X-Ray skull and orbits showed evi­dence of raised intracranial tension and destruction of the sella tursica with calcification posterior to basis­phenoid. There was destruction of the left orbital roof.

Left carotid angiography showed evidence of left temporal lobe tumor with orbital extension.

Other investigations like screening chest, X-Ray chest and spine, sero­logy, E.S.R., haemogram and urine examination showed no abnormality.

The patient was strongly urged to consult a neuro-surgeon which he did after some delay. The neuro-surgeon removed a large tumour from the left fronto-temporal region extending into the orbit. Histopathology proved this to be a Chordoma.

The patient returned to us much re­lieved. He had no headache, no pain in ears and the gait almost restored to normal. By now, unfortunately his vision was extinct completely. The abducent palsy of the left persisted, the proptosis remained the same, though the facial paresis was better. The right fundus now had the picture of complete postpapilloedemic atro­phy. Patient reported with a gaping skull wound though the X-Ray skull, chest, spine showed no metastasis. The wound healed ultimately. The patient is alive but completely blind.

  Discussion Top

The order of precedence of papil­loedema and atrophy is uncertain and depends on the site and size of the tumour. A typical example of such influence is in optic neuro glioma en­tering the cranium. Here the ipsila­teral optic atrophy occurs well in ad­vance of any evidence of the oedema. On the contrary a meningioina may exhibit the oedema on the contrala­teral side before the atrophic changes become manifest. In 1909 PATON re­ported a case of unilateral papillo­edema with contralateral blindness without optic disc involvement. How­ever, two years later frontal lobe tumor was detected during autopsy. In five cases of frontal lobe tumor and one of frontal lobe abscess FOSTER KENNEDY thought the optic atrophy to be due to a toxic factor and papill­oedema to be due to raised intracranial tension. In 1945 JEFFERSON pointed out the possibility of pressure on the optic nerve and its pathway to be the cause of atrophy.

MEHRA et al consider it to occur in about 2% of all cerebral tumors. Depending on the site and size of the tumor, various changes in the two eyes will be found. In the early phase the atrophy may be missed. Early palor, good vision and corresponding field defect on the ipsilateral side with normal disc on the contralateral side is to be expected. Gradual develop­ment of papilloedema on the contrala­teral side with increase in optic atro­phy on the ipsilateral side follows.

Ultimately, the second eye develops postpapilloedemic atrophy. Various causes have been assigned to the con­dition. Tumors are the most common factor.

Amongst the non neoplastic condi­tions, optochiasmal arachnoiditis, sclerosis of the internal carotid artery, syphilitic basal meningitis and Paget's disease of the skull, craniostenosis, tubercular meningitis, frontal lobe ab­scess have been reported.

The tumors are mostly gliomas in connection with frontal lobe, olfactory groove, chiasma, sphenoidal ridge meningioma. Not all such cases de­velop the Foster-Kennedy syndrome. In BYNKE'S (1958) series only 17 out of 1400 such cases and only in 1 out of 180 patients of frontal lobe tumour, this syndrome was present. Similarly in HUBER'S (1961) series 2 out of 25 cases of sphenoid wing tumour and 3 out of 16 cases of meningioma of the olfactory groove, had this syndrome.

  Chordoma Top

It is a rare tumor and arises from the notochord remnant just posterior to the dorsum selle. Because of its location it may cause visual, hypophy­seal and hypothalmic symptoms. It may extend forward into the inter­peduncular cystern and into the nasal sinuses and orbit producing eye motor symptoms. It may extend downwards the foramena magnum producing symptoms from cranial nerve involve­ment and cerebellar ataxia.

  Summary Top

Chordoma situated at the left fron­totemporal site extending into the orbit produced a full blown picture of Fos­ter Kennedy syndrome in a young adult.

The patient presented with papill­oedema, facial paresis and hemipare­sis on the right side; and proptosis, primary optic atrophy and abducent paralysis on the left.


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