Synonyms: Kennedy's phenomenon; Gowers-Paton-Kennedy syndrome
Foster Kennedy's syndrome (FKS) is a rare neurological sign first described in 1911 by Robert Foster Kennedy.1,2 He was a British neurologist, who spent the majority of his working life in America (1884-1952). It consists of:
- Unilateral, ipsilateral optic atrophy, produced by direct pressure on the optic nerve.
- Contralateral papilloedema secondary to raised intracranial pressure (ICP).
- Central scotoma.
- Anosmia.
Pseudo-FKS has also been described, in which there is unilateral optic disc swelling with contralateral optic atrophy in the absence of an intracranial mass.This occurs typically due to bilateral sequential optic neuritis or ischaemic optic neuropathy.3 A case secondary to pachymeningitis (inflammation of the dura mater) has also been reported.4
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Pathogenesis
It is most commonly caused by a tumour on the inferior surface of the frontal lobe. This is usually an olfactory groove meningioma or a medial third sphenoidal wing meningioma.
It has also been reported as a consequence of:
- A metastatic cerebral tumour.5
- Arteriovenous malformation, in which chronic venous hypertension was the likely aetiology.6
- Juvenile nasopharyngeal angiofibroma (a rare benign tumour of the nasopharynx that occurs in adolescent boys with epistaxis and nasal obstruction).7
A review of the 36 previously reported cases of FKS revealed that only eight (22%) of the cases satisfied Foster Kennedy's original hypothesis for the pathogenesis of his syndrome. 12 cases (33%) were probably caused by bilateral optic nerve compression.8 The authors conclude that as more sophisticated imaging permits earlier and more precise diagnosis, future cases of FKS caused by a mass will probably be found to result from bilateral direct optic nerve compression.
Associated symptoms
These include:
- Nausea.
- Vomiting.
- Memory loss.
- Emotional lability, i.e. other frontal lobe signs.
Management and prognosis
Both depend on the underlying cause.
Document references
- Kennedy F; Retrobulbar neuritis as an exact diagnostic sign of certain tumors and abscesses in the frontal lobe. American Journal of the Medical Sciences, Thorofare, N.J., 1911, 142: 355-368
- Stone JL, Vilensky J, McCauley TS; Neurosurgery 100 years ago: the Queen Square letters of Foster Kennedy. Neurosurgery. 2005 Oct;57(4):797-808; discussion 797-808. [abstract]
- Bansal S, Dabbs T, Long V; Pseudo-Foster Kennedy Syndrome due to unilateral optic nerve hypoplasia: a case J Med Case Reports. 2008 Mar 18;2:86. [abstract]
- Tamai H, Tamai K, Yuasa H; Pachymeningitis with pseudo-Foster Kennedy syndrome. Am J Ophthalmol. 2000 Oct;130(4):535-7. [abstract]
- Yildizhan A; A case of Foster Kennedy syndrome without frontal lobe or anterior cranial fossa involvement. Neurosurg Rev. 1992;15(2):139-42.; Neurosurg Rev. 1992;15(2):139-42. [abstract]
- Liang F, Ozanne A, Offret H, et al; An atypical case of Foster Kennedy syndrome. Interv Neuroradiol. 2010 Dec;16(4):429-32. Epub 2010 Dec 17. [abstract]
- Aga A; Juvenile nasopharyngeal angiofibroma presenting as Foster Kennedy Syndrome. Ethiop Med J. 2001 Jul;39(3):251-60. [abstract]
- Watnick RL, Trobe JD; Bilateral optic nerve compression as a mechanism for the Foster Kennedy syndrome. Ophthalmology. 1989 Dec;96(12):1793-8.; Ophthalmology. 1989 Dec;96(12):1793-8. [abstract]
Internet and further reading
- Yeh WY, Cheng CK, Peng PH, et al; Foster Kennedy Syndrome in a Case with Retinitis Pigmentosa. Ophthalmic Surg Lasers Imaging. 2010 Mar 9:1-3. doi: [abstract]
Acknowledgements
EMIS is grateful to Dr Laurence Knott for writing this article and to for earlier versions. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2011.Document ID: 1704
Document Version: 22
Document Reference: bgp1224
Last Updated: 21 Apr 2011