Foster Kennedy Syndrome Research Articles

Third Ventricular Ependymoma Mimicking Foster Kennedy Syndrome- A Case Report

Authors' contributions This work is carried out in collaboration of all authors. Authors ELT and RK designed the study, wrote the first draft of the manuscript and managed the literature search. Authors RK, WHWH and LSAT revised it critically for intellectual contents. Authors ELT, RK, WHWH and TLK were involved in the assessment and treatment of the patient. All authors read and approved the final manuscript. ABSTRACT Aims: To report a case of a third ventricular tumour mimicking Foster Kennedy Syndrome in a young adult. Presentation of Case: A 21-year-old female presented with bilateral blurring of vision with preceded by generalized headache, nausea and vomiting. Fundoscopy revealed optic nerve atrophy of the right eye and a swollen optic disc on the left in keeping with features of Foster Kennedy Syndrome. MRI of the brain revealed a third ventricular tumor extending into the suprasellar region with hydrocephalus. Surgical excision of the tumour was done and the subsequent histopathological report confirmed it to be a clear cell ependymoma. Discussion: Foster Kennedy syndrome is a rare clinical constellation describing a pattern of ocular findings typically related to extraaxial tumours involving the anterior skull base. It is characterized

Foster Kennedy syndrome

No abstract available

Wilhelm Uhthoff (1853–1927)

Wilhelm Uhthoff (Fig. 1) was a German ophthalmologist, especially interested in neurology. He was born on June 31, 1853, in Klein-Warin in Grand Duchy of Mecklenburg-Schwerin (now Mecklenburg-Vorpommern). He was raised in the countryside, as one of nine siblings. Because of the poor financial situation of his family he could not expect any financial means to support his education. Thus, working 7 days a week was required later on to pay off the loans obtained to cover education-linked expenses [1]. Fig. 1 Wilhelm Uhthoff (1853–1927) He studied medicine in Tubingen, Gottingen, Rostock and Berlin. He defended his doctoral dissertation in 1877 in Berlin. These years marked the initiation of collaboration with Rudolph Virchow (1821–1902), co-researcher, but also colleague at Breslau University thereafter. In 1878, Uhthoff began ophthalmology residency and became a research assistant at Heinrich Leopold Schoeler’s (1844–1918) clinic in Berlin [2]. Meanwhile, at Helmholtz Physics Institute, he carried out work on light luminance and visual acuity [3]. His interest in neuro-ophthalmology was expressed by establishing consultations at Carl Westphal neurology clinic of Charite Hospital in Berlin [3]. Among his co-workers Adolf Wallenberg (1862–1949), Hermann Oppenheim (1858–1919), Carl Moehli (1849–1919) and Ernst Siemerling (1857–1931) can be listed [2]. Uhthoff shared a bacteriological research interest with his eldest student, Theodor Axenfeld (1867–1930). In 1885, he obtained senior doctor lecturer title and 5 years later was appointed Ordinary Professor to the Chair of Ophthalmology in Marburg. In 1896, he accepted the position of the Head of the University Eye Clinic and moved to Breslau. Advancing his academic career, he was nominated for rector of Friedrich Wilhelm Silesian University (Schlesische Friedrich-Wilhelms-Universitat zu Breslau) and, subsequently, University of Breslau in 1908. Uhthoff was a devoted researcher and lecturer—many case reports of his authorship established the basis of modern neuro-ophthalmology. His research covered multiple fields, including eye anatomy and pathology, relation between light luminance and visual acuity, alcohol-induced loss of vision, color perception, visual acuity, sclera anatomy, cornea and conjunctiva pathology as well as difference in ophthalmologists’ and neurologists’ perception [4]. In 1890, he observed and described a novel symptom of reversible blurriness of vision after a strenuous physical exercise among multiple sclerosis patients. This symptom is known today as Uhthoff’s phenomenon (known also as Uhthoff sign or syndrome). In 1915, he described ophthalmological signs and symptoms of brain tumors, improving the picture of Foster-Kennedy syndrome [5]. During the 1st World War, while examining soldiers with head injuries, in cooperation with Sir Gordon Morgan Holmes (1876–1965), he worked on cortical representation of retinal areas [6]. He also described retinal detachment management, ophthalmological manifestations of intoxications and was an advocate for blind patients [4]. Uhthoff retired in 1923, however, he did not cease his scientific activity, but continued working on publications on acquired research material. He died suddenly of a heart attack as a complication of influenza on March 21, 1927, in Breslau [3].

Foster Kennedy Syndrome

Foster Kennedy Syndrome

Pseudo Foster Kennedy Syndrome secondary to uncontrolled hypertension and diabetes mellitus: A case report

Pseudo-Foster Kennedy Syndrome is described as unilateral optic disc swelling with contra lateral optic atrophy in the absence of an intracranial mass causing compression of the optic nerve. This occurs typically due to bilateral sequential optic neuritis or ischemic optic neuropathy. We describe a case of pseudo-Foster Kennedy Syndrome in a 37-year-old male with unilateral papilledema secondary to malignant hypertension and pre-existing ischemic optic neuropathy in other eye preventing transmission of raised intracranial pressure to the optic nerve. Hypertension and diabetes mellitus (DM) play a significant role in pathogenesis of ischemic optic neuropathy. There is a greater correlation in patients with small disc and little to no cupping. The disorder commonly occurs in the 40-65 yrs age group. Our case is an example of Pseudo-Foster Kennedy syndrome where papilledema in one eye was associated with uncontrolled hypertension and disc pallor in fellow eye was secondary to ischemic optic neuropathy.

Foster Kennedy Syndrome Due to Meningioma Growth during Pregnancy

Tumors of the olfactory groove may cause unilateral optic atrophy with contralateral papilledema and anosmia (Foster Kennedy syndrome). We describe a case of a young pregnant woman with Foster Kennedy syndrome due to an olfactory groove meningioma.

Primary meningeal melanocytoma of the anterior cranial fossa: a case report and review of the literature

BackgroundPrimary meningeal melanocytoma is a rare neurological disorder. Although it may occur at the base of the brain, it is extremely rare at the anterior cranial fossa.Case presentationA 27-year-old man presented with headache and diplopia at our department. Fundoscopy showed left optic nerve atrophy and right papilledema consistent with Foster-Kennedy syndrome. Neurological exams were otherwise normal. A left frontal irregular space-occupying lesion was seen on magnetic resonance imaging (MRI), and enhancement was shown on contrast-enhanced computed tomography (CT) scan. CT angiography (CTA) revealed vascular compression around the lesion. Prior to surgery, meningioma was diagnosed and gross tumor removal was performed. On postoperative pathohistological exam, the tumor proved to be a meningeal melanocytoma, WHO grade I. No skin melanoma was found. After surgery, the patient received radiation therapy. No tumor was seen on follow-up MR images six months after surgery. The patient was well after two and a half years, and there was no tumor recurrence on the follow-up CT.ConclusionsThis case of primary meningeal melanocytoma located at the anterior cranial fossa is very rare. Although primary meningeal melanocytoma is benign, it may behave aggressively. Complete surgical resection is curative for most cases. Radiation therapy is important to prevent relapse of the tumor, especially in cases of incomplete surgical resection.

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

Anahtar kelimeler: Foster Kennedy Sendromu; optik atrofiler; manyetik rezonans goruntuleme; norolojik muayene belirtilerin artmasi ve karsi taraftaki gozdeki odemin atrofi ye ilerlemesi gibi gec donem komplikasyonlarin ortaya ciktigini saptadik. Bu sendromun nadiren gorulmesi, menenjiomun dev boyutlarda olmasi, hastanin aralikli olarak detayli norooftalmolojik ve radyolojik incelemelerinin bulunmasi nedenleriyle olgunun sunumunu uygun gorduk.

An Aggressive Sphenoid Wing Meningioma Causing Foster Kennedy Syndrome

Foster Kennedy syndrome is a rare neurological condition with ophthalmic significance that can manifest as acute visual loss. It is classically characterised by unilateral optic nerve atrophy and contralateral papilledema resulting from an intracranial neoplasm. Physicians should consider Foster Kennedy syndrome in patients who present with visual loss and who have a history of intracranial neoplasm. In addition to ophthalmologic examination, neuroimaging is essential for the diagnosis of Foster Kennedy syndrome.

Pseudo-Foster Kennedy syndrome in a young woman with meningioma infiltrating the superior sagittal sinus

The original Foster Kennedy syndrome results from the uncomon combination of unilateral optic disc swelling in one eye and ptic atrophy in the contralateral; it is usually due to a frontal obe tumor compressing the optic nerve [1]. In the absence of an ntracranial mass these findings may be labeled as pseudo-Foster ennedy syndrome. The pathogenesis of the optic disc pallor is elieved to be secondary to the direct compression of the prehiasmatic optic nerve fibers; whereas, the disc edema in the fellow ye is attributed to increased intracranial pressure from the spaceccupying mass. Pseudo-Foster Kennedy is a more frequent clinical icture, resulting from more remote ischemia or demyelination n one eye, with subsequent atrophy, and often persistent visual oss, with new ischemia or demyelination in the second eye, with ew visual loss [2]. Many mechanisms have been proposed for his syndrome including: (i) direct but asymmetric compression of oth optic nerves, with severe compression causing pallor, and less evere compression causing optic disc edema owing to impaired xoplasmic flow; (ii) chronic increased intracranial pressure iniially causing bilateral papilledema, with one optic disc eventually eveloping pallor as the result of axonal death and the other optic isc remaining swollen [3]. Herein we present a case of Pseudo-Foster Kennedy syndrome ccurring in a young woman with meningioma infiltrating the

Foster Kennedy syndrome: papilledema in one eye with optic atrophy in the other eye

A 36-year-old man presented to the emergency department because of gradual blurring of vision in his right eye over 20 days and progressive loss of vision in the left eye over the previous eight months. One year earlier, he had started taking sodium valproate for morning migraines with only a

An Atypical Case of Foster Kennedy Syndrome

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 probable etiology.

Einseitiges Papillenödem und kontralateraler Visusverlust

A 46-year-old woman presented with a 4-day history of headache, dizziness and blurred vision in the left eye and a 1-year history of neck pain. Fundoscopy revealed a pale optic disc in the left eye and a swollen optic disc in the right eye. Furthermore a bilateral anosmia was evident. Cranial magnetic resonance imaging (MRI) showed a mass in the anterior cranial fossa, which was classified as a WHO grade I endotheliomatous meningeoma. A Foster Kennedy syndrome was diagnosed.

An unusual presentation of subfrontal meningioma: a case report and literature review for Foster Kennedy syndrome

Intern Emerg Med (2011) 6:267–269 DOI 10.1007/s11739-010-0437-y CE - MEDICAL ILLUSTRATION An unusual presentation of subfrontal meningioma: a case report and literature review for Foster Kennedy syndrome Shahram Lotfipour • Kris Chiles • J. Akiva Kahn Tareg Bey • Scott Rudkin Received: 17 December 2009 / Accepted: 13 July 2010 / Published online: 26 August 2010 O SIMI 2010 Introduction Foster Kennedy syndrome, named after neurologist Robert Foster Kennedy (1884–1952), describes unilateral ipsilat- eral optic atrophy and contralateral papilledema from an intracranial mass. This syndrome is unreliably associated with anosmia and ipsilateral proptosis [1]. It originates from variety of intracranial pathologies, but most often a subfrontal mass. We present a case of Foster Kennedy syndrome and review its etiology, pathology and incidence in intracranial tumors. Case report A 47-year-old woman was brought in by her family to the Emergency Department (ED) for psychiatric care. The patient had been homeless for 17 years prior to the visit, but had recently been taken in by her family, and brought in for evaluation of her personality changes. She denied any recent S. Lotfipour T. Bey S. Rudkin Irvine School of Medicine, University of California, Orange, USA K. Chiles Highland General Hospital, Oakland, USA J. A. Kahn Thomas Jefferson University, Philadelphia, USA S. Lotfipour (&) Department of Emergency Medicine and Public Health, Clinical Science Education, University of California, Irvine School of Medicine, 200 S. Manchester Avenue, Suite 710, Orange, CA 92868, USA e-mail: SHL@uci.edu head trauma. She admitted to abusing crack cocaine for 13 years with her last use 4 months ago. She denied any trouble with ambulation, dizziness, and changes in hearing or other alterations in sensation. She denied any suicidal or homicidal ideation. The patient denied any auditory halluci- nations, but did report that she had been experiencing visual hallucinations and visual disturbances for at least 6–8 months. She reported complete blindness in the left eye, and shadow perception in her right for an unknown length of time. Her past medical history was notable for major depression. The patient did not have a previous history of hallucinations or psychosis, and had never been hospitalized for psychiatric reasons. The patient was not on any medica- tions, and was allergic to penicillin and codeine. The gyne- cologic, surgical and family histories were noncontributory. Initial vital signs were: temperature 36.9°C, pulse 86 beats/min, blood pressure 95/63 mm/Hg, respiratory rate 16 breaths/min, and oxygen saturation 100% on room air. On physical examination, the patient was alert and oriented to person, place and time. Her left pupil was nonreactive to direct light with a normal consensual light response and inability to count fingers with either eye. Extraocular movements were intact and cranial nerves IV through XII were normal. Further evaluation revealed she had anosmia, left optic nerve atrophy and right papilledema. Laboratory studies were normal and urine toxicology was negative. Per hospital protocol initially a non-contrast computed tomography (CT) of the head revealed a large homogenous mass in the anterior cranial fossa (Fig. 1) measuring 8.0 9 6.1 cm. The mass had a calcified rim, and had eroded into the ethmoid sinus and bilateral orbits. A magnetic resonance imaging (MRI) confirmed the diagnosis of a subfrontal meningioma (Fig. 2). The patient was started on phenytoin for seizure pro- phylaxis and dexamethasone to reduce cerebral edema. She

Foster Kennedy Syndrome in a Case with Retinitis Pigmentosa.

A 57-year-old woman suffering from long-term visual disturbance due to retinitis pigmentosa noted an even more severe deterioration of her left vision for several months. On ophthalmologic examination, her vision was 1/60 in the right eye and light perception (LP) in the left eye. An RAPD sign was noted in her left eye. Bilateral fundus revealed the typical appearance of severe retinitis pigmentosa. The optic disc of her right eye was markedly swollen, whereas that of the left eye was pale. Under the impression of the Foster Kennedy syndrome, a magnetic resonance imaging (MRI) study was arranged revealing a well-encapsulated round mass with a contrast enhancement of about 4.45 cm in diameter located in the left frontal lobe. The patient might have ignored the visual disturbance in her left eye caused by tumor compression because of her illness of retinitis pigmentosa, which had caused her visual disturbance since childhood.

Intracranial Meningiomatosis Causing Foster Kennedy Syndrome by Unilateral Optic Nerve Compression and Blockage of the Superior Sagittal Sinus

The original description of the Foster Kennedy syndrome included the clinical triad of optic disc pallor in one eye, optic disc edema in the other eye, and reduced olfaction caused by space-occupying anterior fossa masses. The optic disc pallor was attributed to direct compression of the intracranial optic nerve, the optic disc edema to increased intracranial pressure from mass effect, and the reduced olfaction to direct compression of the olfactory nerve. We report a patient with the ophthalmic features of the Foster Kennedy syndrome from meningiomatosis. A meningioma compressed one optic nerve to cause impaired visual function. Convexity meningiomas compressed the superior sagittal sinus to impair cerebral venous drainage, increased intracranial pressure, and papilledema in the other eye. This is the first report of the Foster Kennedy syndrome caused by this mechanism.

Pseudo-Foster Kennedy Syndrome due to unilateral optic nerve hypoplasia: a case report

IntroductionPseudo-Foster Kennedy Syndrome is described as unilateral optic disc swelling with contralateral optic atrophy in the absence of an intracranial mass causing compression of the optic nerve. This occurs typically due to bilateral sequential optic neuritis or ischaemic optic neuropathy.Case PresentationWe describe a case of pseudo-Foster Kennedy Syndrome in a two year old boy with unilateral papilloedema due to a congenital optic disc anomaly in one eye preventing transmission of raised intracranial pressure to the optic nerve.ConclusionFrom our findings we conclude that congenital optic nerve hypoplasia is a cause of pseudo-Foster Kennedy Syndrome.

Neurosurgery 100 Years Ago: The Queen Square Letters of Foster Kennedy

The prominent New York City neurologist Foster Kennedy (1884-1952) trained at London's Queen Square from 1906 to 1910. He was exposed to a number of eminent neurologists including, Sir Victor Horsley and other surgeons. A previously published but little known group of Kennedy's personal letters written during his neurological training is reviewed in light of their historic neurosurgical context. These often entertaining although at times unflattering letters capture the elation and frustration of neurosurgical experience during that important developmental period. Descriptions of the personalities involved give rare insight to this era. The Foster Kennedy syndrome--homolateral optic atrophy and contralateral papilledema with an inferior frontal tumor--was characterized under the stimulating support of Gowers and Horsley.

Victor Horsley's contribution to the Foster Kennedy Syndrome

Although Foster Kennedy is the name given to the syndrome localizing an intracranial tumour with respect to papilloedema, it is important to recognize how Victor Horsley was one of the strongest proponents in the usefulness of that sign. Not only did he describe the constellation of findings before Kennedy did, he was also probably one of the people who had influenced Kennedy the most during the latter's time at the National Hospital for Nervous Diseases at Queen Square. It is therefore appropriate that Victor Horsley's characterization in 1910 of the findings that were later recorded as the Foster Kennedy syndrome, and that his altruistic encouragement of Kennedy's publication of the findings, receive recognition and appreciation in the medical and historical community.

Pachymeningitis with pseudo–Foster Kennedy syndrome

PURPOSE: To report a case of pachymeningitis with pseudo–Foster Kennedy syndrome in a patient who was positive for perinuclear antineutrophil cytoplasmic antibody. METHODS: Case report. A 44-year-old man was examined for headache and diplopia. RESULTS: Left eye showed limitation of abduction. Ocular fundus, computed tomography (CT), and magnetic resonance imaging (MRI) of the head and orbits were normal. The diplopia subsided spontaneously. Six months later, he noticed sudden visual loss in the left eye. The left eye showed optic disk atrophy and episcleritis, and the right eye showed papilloedema. Computed tomography and MRI exhibited thickened dura mater. Serum perinuclear antineutrophil cytoplasmic antibody level was highly increased. CONCLUSION: Pachymeningitis with ocular involvement sometimes requires repeated CT or MRI for diagnosis. This disorder may be caused by microvasculitis.