An Atypical Case of Foster Kennedy Syndrome

Abstract

<jats:p> Foster-Kennedy syndrome was described in 1911 as an ophthalmologic manifestation of compression by a solid tumor in the frontal area with intracranial hypertension (ICHT). We describe a peculiar case of Foster-Kennedy syndrome associated with an arteriovenous malformation in which neither optic nerve compression nor ICHT was obvious. We discuss the different pathogenic mechanisms to explain this case, for which a chronic venous hypertension was the most probabile etiology. </jats:p>

Foster-Kennedy syndrome – a case report

“…Type 1 is the classic presentation with direct compression of the optic nerve and elevated intracranial pressure. Type 2 involves bilateral direct nerve compression without features of intracranial hypertension, while type 3 encompasses cases with- out direct nerve involvement but with chronic intracranial hypertension [5].…”

“…In the edematous eye, on the other hand, visual acuity ranged from hand movement to 1.0, and in the majority of cases surgical treatment resulted in improved vision [2,3,7]. The degree of improvement depends on several factors, the most important of which appears to be the duration of the edema phase [5].…”

Clinicoradiological follow-up of a patient with Foster Kennedy syndrome: a case report.

“…4 Yayınlanmış Foster Kennedy olgularının bazıları frontal lob abseleri, hipofi z adenomları, anevrizmalar, kraniyofarinjiomlar, anjiyofi bromlar, arteriyovenöz malformasyonlar ve nöroblastomlara baglı gelişir-ken, birçoğunun da nedenin (olgumuzda olduğu gibi) menenjiom olduğu saptanmıştır. 3,[5][6][7] Menenjiomların sıklıkla bu sendroma neden olması hem bu tümörün insidansının yüksek olması, hem de en sık lokalizasyonunun beynin ön bölgeleri (parasagittal dura, sfenoid kanat, olfaktor oluk ve planum sfenoidale) olmasıdır. 8 Menenjiomlar ne kadar büyük olursa, yaptığı beyin parankimi ödemi de o kadar geniş olur.…”