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Year : 1965  |  Volume : 13  |  Issue : 2  |  Page : 75-78

Foster-kennedy syndrome in a case of olfactory-groove meningioma

Dept. of Neurology and Neurosurgery, Institute of Post-Graduate Medical Education & Research, Chandigarh, India

Date of Web Publication21-Feb-2008

Correspondence Address:
O N Markand
Dept. of Neurology and Neurosurgery, Institute of Post-Graduate Medical Education & Research, Chandigarh
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How to cite this article:
Markand O N, Chandrakar K L. Foster-kennedy syndrome in a case of olfactory-groove meningioma. Indian J Ophthalmol 1965;13:75-8

How to cite this URL:
Markand O N, Chandrakar K L. Foster-kennedy syndrome in a case of olfactory-groove meningioma. Indian J Ophthalmol [serial online] 1965 [cited 2021 Jul 31];13:75-8. Available from: https://www.ijo.in/text.asp?1965/13/2/75/39221

Paton (1909) was the first to report a case of frontal lobe tumour causing blindness in one eye and papilloedema in the other. The blind eye did not show optic atrophy, however, although compression of the optic nerve by the tumour was demonstrated at autopsy. Two years later, Foster-Kennedy (1911) reported five cases of frontal-lobe tumour and one case of frontal lobe abscess, who had primary optic atrophy on the side of the lesion with papilloedema on the contralateral side. Since that time, the combination of pri­mary optic atrophy in one eye and papilloedema in the other, has been known as Foster-Kennedy Syndrome.

Subsequently, the syndrome has been described in tumours other than those of the frontal lobe and also in non-neoplastic intracranial lesions. Cushing (1927) reported this syndrome in association with meningioma of the olfactory groove. Other intracranial neoplasms producing this syndrome are sphenoidal ridge meningioma, (Van der Hoeve and Kijne 1943)-meningioma of the falx cerebri (Masters - 1953) and tumours of the quadrigeminal plate, (Globus - 1931), cerebellum (Cusick-1938), third ventricle (Rey-non-1956) and premotor cortex (Gar­cia-Miranda--1946).

Among the non-neoplastic conditions associated with this syndrome, are optochiasmal arachnoiditis. Gas- kin and Schlesinger-1948, Francois and Neetens-1955, aneuysmal dilation of internal carotid artery (Tassman-1944) sclerosis of internal carotid artery (Martell--1955), syphilitic basal meningitis and Pagets disease of the skull.

A typical case of Foster-Kennedy Syndrome associated with olfactory groove meningioma is described be­low.

  Case Report Top

Mr. B.S. 42 years male was referred from a Medical college Hospital to the neurological service of the Institute of Postgraduate Medical Education and Research, Chandigarh, on 2nd March, 1964. The history of the illness was obtained from the brother of the pati­ent because the patient himself was not in a state to offer correct history. The patient was known to have head­ache of moderate severity for the last two years. For the last six months he was having grandmal type of epilepsy without any feature of localisation. These attacks had a frequency varying from 1-3 per month. Two months back the patient started noticing diminished acuity of vision, first in the left eye and a few days later in the right eye. From the same time an alteration in behavi­our of the patient was noticed by his relatives. He would talk irrelevantly and would void urine in bed. For less than a month the patient was complete­ly blind. The patient never complained of any alteration in the perception of smell to his brother.

Clinical examination revealed a moderately built, middle aged male with a vacant look fully disoriented in time and space and not answering to questions. Pulse was 68 per minute, respiration 18/min. and blood pressure 130/90 mm. of mercury. There was no significant lymphadenopathy. There was no dependent oedema. Naso-pharyngeal examination did not re­veal any abnormality. Respiratory system and cardiovascular system did not reveal any abnormality. The liver and spleen were not palpable.

Neurological examination showed markedly impaired mental functions of the patient. He was disoriented about time, place and persons. Occasionally he used to talk irrelevantly and laugh without reason. He was fully consci­ous, and his speech was normal.

Cranial nerve examination showed loss of sense of smell on both the sides. There was total loss of vision in both the eyes. Pupils were widely dilated and did not react to light. Fundoscopy showed gross papilloedema with hemorrhages on the left side and ap­pearance of primary optic atrophy on the right. There was no evidence of oculomotor or facial nerve palsy. Other cranial nerves did not show any gross abnormality of function. A com­plete examination of motor and sensory functions was not possible but there was no evidence of paralysis or anaes­thesia in the limbs. Plantar reflex was flexor on both sides. Hoffmann's sign and grasp reflex were elicitable on both sides. Abdominal and cremastric reflexes were normal. Gait was normal and there was no ataxia.

The above clinical features of loss, of sense of smell, right sided optic at­rophy, left sided papilloedema, bilater­al blindness, grandmal epilepsy and dementia suggested a supratentorial space occupying lesion, either a frontal lobe tumour or olfactory groove meningioma.

  Investigations Top

The routine investigations showed: haemoglobin, 10.5 gm per cent; total leucocyte count, 9600/cmm; differen­tial count: polymorphs 64 per cent: lymphocytes, 36 per cent; and erythrocyte sedimentation rate, 18 mm. 1 st hour Wintrobe. Urine and stool did not show any abnormality. Skiagram of the skull showed evidence of raised intracranial pressure by demonstrating sutural diastasis and decalcification of the post clinoid processes.

Because the patient had right sided optic atrophy, right carotid angiogram was done by percutaneous technique. It showed the following features: (1) In anteroposterior view, [Figure - 1] there was a contralateral shift of the anterior cerebral artery with a tumour -Blush" near the middle extending on both sides, more on the right. (2) In the lateral view the anterior cerebral artery showed a backward displacement with flattening of the carotid syphon. A faint tumour "blush" was seen in the region of anterior cranial fossa [Figure - 2]. In the venous phase the tumour "blush" was well demar­cated in the anterior cranial fossa and had extended as far back as the sella turcica [Figure - 3]. Feeding vessels from the external carotid circulation could not be demonstrated in the an­giograms. The radiographic pictures were very much suggestive of olfactory groove meningioma.

The patient was discharged from the hospital against medical advice on 11-3-64 after 9 days of hospitalisation.

  Comment Top

The patient had a typical Foster- Kennedy Syndrome most probably as a result of an olfactory groove menin­gioma, arising on the right side and invading the anterior fossa on that side as well as extending to the oppo­site side. The presence of bilateral anosmia favours the concept of a tumour primarily involving the olfac­tory tract. Dementia epilapsy, incon­tinence of urine and the presence of bilateral grasp reflex were, presumably due to involvement of the frontal lobes and partially to intracranial hyperten­sion.

Though the association of Foster- Kennedy Syndrome with olfactory groove meningioma was described as early as 1927 by Cushing, subsequent reports have shown this association to be quite rare. Thus, Hartmann et al (1937) in their report on ocular mani­festations in 16 cases of olfactory groove meningioma encountere,d no typical example of the Foster-Kennedy Syndrome, though they observed two cases showing variants of this synd­rome.

As regards pathogenesis, Foster- Kennedy (1911) believed that the ipsi­lateral primary optic atrophy was the result of true retrobulbar neuritis while the contralateral papilloedema was due to raised intracranial pressure associat­ed with intracranial space occupying lesion. Jefferson (1945), however, em­phasized that the ipsilateral optic atropy was the result of direct com­pression (and not due to retrobulbar neuritis) of the optic nerve or optic pathways by the intracranial lesion and the intracranial hypertension produced papilloedema on the opposite side. Sub­sequent observations have confirmed the view of strangulation of optic nerve as the cause of optic atrophy in Foster- Kennedy Syndrome.

The localising value of this synd­rome is definitely limited because it has been seen in tumours well re­moved from anterior fossa and also in certain non-neoplastic conditions in the neighbourhood of optic chiasma. These exceptions are, however, rare and seem to emphasize that in almost all instances a Foster-Kennedy Synd­rome is found to be associated with an expanding lesion of the basofrontal region or of the anterior cranial fossa.[18]

  Summary Top

A case of Foster-Kennedy Syndrome most probably due to olfactory groove meningioma is described. The litera­ture is briefly reviewed.

  Acknowledgment Top

Thanks are due to Dr. S. S. Anand, Director of the Institute for allowing us to publish this case. We are also thankful to Dr. D. R. Gulati, Addi­tional Professor of Neurosurgery, for his valuable suggestions.

  References Top

Borsello. G.: (1948) Atti d. 37 Con­gress Soc. Oftal. ital.. 10: 554.  Back to cited text no. 1
Bynke. Hans: (1958) Acta Ophth. 36: 129.  Back to cited text no. 2
Cushing. H.: (1927). Lancet, 1:1324.  Back to cited text no. 3
Cusick, P. L.: (1938) Proc. Staff Meet. Mayo Clinic, 13: 433.  Back to cited text no. 4
Foster-Kennedy: (1911) Am. J.M.Sc., 142: 355.  Back to cited text no. 5
Francois, J., and Neetens, A. (1955) Ann. d'ocul., 188: 219.  Back to cited text no. 6
Garcia-Miranda. A. (1946) Ophthal­mologica. 112: 72.  Back to cited text no. 7
Globus, J. H.: (1931) Arch. Ophth. 5: 418.  Back to cited text no. 8
Hartmann. E. David M., and Desvignes. P.: (P.: 1937) Quoted by Walsh. F.B., in "Clinical Neuro-Ophthalmology" page 996 Williams and Wilkins Com­pany. Baltimore. second edition, 1957.  Back to cited text no. 9
Jefferson, G.: (1945) Trans. Soc. U. Kingdom. 65: 262.  Back to cited text no. 10
Martell. A.: (1955) Riv. Otoneuro­-Oftal. 30: 487.  Back to cited text no. 11
Masters, S.: (1953) Am. J. Ophth., 36: 983.  Back to cited text no. 12
Montressor. D.: (1951) An. ottol. & Ocul., 77: 343, 1951.  Back to cited text no. 13
Paton, L.: (1909) Brain. 32: 65.  Back to cited text no. 14
Reynon. M.: (1956) Ann. d'ocul., 189: 596.  Back to cited text no. 15
Tassman. I.: (1944) Arch. Ophth., 32: 125.  Back to cited text no. 16
Van der Hoeve, G. J.. and Kijne, J.: (1943) Indian Med. Gazette. 78: 242.  Back to cited text no. 17
Yaskin, E. H., Schlesinger, N.S.: (1942) Arch , Ophth.. 28: 704.  Back to cited text no. 18


  [Figure - 1], [Figure - 2], [Figure - 3]


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