|Year : 1973 | Volume
| Issue : 1 | Page : 32-33
Foster Kennedy syndrome
Prabha Bhura, RK Mishra
Department of Ophthalmology, Medical College, Jabalpur, India
Department of Ophthalmology, Medical College, Jabalpur
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Bhura P, Mishra R K. Foster Kennedy syndrome. Indian J Ophthalmol 1973;21:32-3
Foster Kennedy syndrome is a well known condition of uncommon occurrence showing optic atrophy on one side with papilloedema on the other.
| Case Report|| |
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|| |
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|| |
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|| |
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.