Foster Kennedy Syndrome Research Articles

Sarcomatous Change in Polyostotic Paget's Disease-A Diagnostic Conundrum

This is a report of a 56-year-old man presented to highlight the clinical features and diagnostic difficulties of Paget's disease in our environment. The patient had a four year history of intractable body pains and at different times had pathological fracture, loss of vision, conductive hearing loss, frequent intermittent anaemia requiring blood transfusion, paraparesis, one sided headache, cardiac failure and suspected Foster Kennedy syndrome. An earlier bilateral orchidectomy was done for suspected metastatic carcinoma of the prostate following markedly elevated acid phosphatase and ESR in the presence of enlarged hard prostate but a trucut biopsy of the gland later showed no evidence of malignancy. A multidisciplinary clinical assessment along with sequential ancillary test, roentgenography and bone marrow study helped to arrive at the eventual diagnosis (Nig J Surg Res 2000; 2:88-91) KEY WORDS: Paget's disease, Sarcomatous change

Fusiform aneurysms (dolichoectasia) of the internal carotid artery as cause of optic nerve damage

Dolichoectasia of cerebral vessels most often occurs in middle-aged or elderly patients, also occasionally in children and in subjects with neurofibromatosis type NF-i. It seems that less atherosclerosis but severe deficiency of reticular fibers in the media associated with extensive defects in the elastic lamina represents the main factor in the pathogenesis of these ectasias. In contrast to saccular aneurysms, the fusiform aneurysms never cause subarachnoid hemorrhage. Those originating from the internal carotid artery produce damage to the optic nerve by direct pressure or by impairment of the circulation of nutrient vessels. Visual loss may be slowly progressive or acute, affecting one eye weeks or years before the other. Visual field defects are not specific: altitudinal, temporal, constriction, central or cecocentral scotomas. Progressive optic atrophy on the affected side is the rule; sometimes papilledema on the other side can mimick a Foster-Kennedy syndrome. The treatment possibilities are discussed: for example, surgical excision of the ectatic vessel region, decompression of the optic nerve by separation from the ectatic vessel (interposition of muscle tissue), or unroofing the optic canal and subsequent cutting of the dural fold and the dural sheath of the optic nerve.

Diagnosis and Management of Temporal Arteritis: A Review and Case Report

Temporal arteritis is an insidious disease which, if not recognized and treated with high-dosage oral prednisone or intravenous prednisolone, can result in unilateral or even total blindness due to anterior ischemic optic neuropathy (AION) or closure of the central artery of the retina. Unfortunately, the symptoms and clinical signs of temporal arteritis mimic those of a number of other conditions including angle-closure glaucoma, hypertension, migraine, trigeminal neuralgia, temporomandibular joint syndrome, carotid artery occlusive disease, Foster-Kennedy syndrome, and nonarteritic AION. When a patient complains of a severe pain in the temporal region, along with scalp tenderness and a feeling of malaise or depression--with or without episodes of transient loss of vision--he or she should be referred for a diagnostic work-up which includes an erythrocyte sedimentation rate and a temporal artery biopsy. We present here a review of the recent literature concerning temporal arteritis, followed by a report of an unusual case in which high-dosage prednisone therapy was effective in relieving the patient's symptoms and lowering the sedimentation rate in spite of a negative temporal artery biopsy.

Pituitary adenoma presenting as the Foster-Kennedy syndrome.

A 27-year-old man presented to the casualty department with visual failure. Clinically he demonstrated the Foster-Kennedy syndrome. Computed tomography revealed a large space-occupying lesion which was subsequently shown to be a pituitary adenoma. The literature is reviewed and possible mechanisms of the Foster-Kennedy syndrome are discussed.

Foster Kennedy syndrome caused by an extensive pituitary adenoma

A 28-year old man presented with decreased vision and a bitemporal hemianopia. Magnetic resonance (MR) imaging demonstrated what appeared to be an enlarged optic chiasm and, on T2-weighted images, hypersignal extending along the optic tracts. This was felt to represent an intrinsic chiasmal mass, most likely a chiasmal glioma. Biopsy specimens from the first craniotomy were nondiagnostic. With continued visual failure, the patient underwent a second operation, and the correct diagnosis of craniopharyngioma was established. This article emphasizes the difficulties encountered with neuroradiologic evaluation and histopathologic study of craniopharyngioma.

Foster Kennedy Syndrome and Optociliary Shunt Vessels in a Patient with an Olfactory Groove Meningioma

A 48-year-old woman complained of acute loss of vision in her right eye. Ophthalmoscopically, the right optic disk appeared pale, and abnormally dilated vessels were noted on the disk. The left optic disk was reddish and swollen. Fluorescein angiography revealed abnormal vessels on the right optic disk that might be venous. The patient had right-sided anosmia. Computed tomography and magnetic resonance imaging showed a lesion in the frontal lobe that was deviated to the right and attached to the olfactory groove. A histopathologic study of the excised specimen disclosed a meningioma. We believe that this patient with olfactory groove meningioma represents a rare case of Foster Kennedy syndrome and optociliary shunt vessels.

Bilateral Optic Nerve Compression as a Mechanism for the Foster Kennedy Syndrome

An 11-year-old boy with a juvenile nasopharyngeal angiofibroma developed optic disc pallor in one eye and optic disc edema in the other eye (Foster Kennedy Syndrome [FKS]). The mechanism was believed to be bilateral, asymmetric optic nerve compression. Review of the 36 previously reported cases of FKS revealed that 12 cases (33%) were probably also caused by bilateral optic nerve compression. Only eight (22%) of the cases satisfied Foster Kennedy's original hypothesis for the pathogenesis of his syndrome, namely, direct compression of one optic nerve causing atrophy and increased intracranial pressure causing contralateral papilledema. In 15 (41%) reported cases of FKS, descriptions were inadequate to determine a mechanism, while two (5%) were probably caused by long-standing increased intracranial pressure without direct optic nerve compression. The authors believe that as sophisticated imaging permits earlier diagnosis and more precise localization, most future cases of FKS caused by mass lesions will be found to result from bilateral direct optic nerve compression.

Huge meningioma in a child

A case of a 6-year-old boy with a large meningioma is reported. The patient had an enlarged head, the Foster Kennedy syndrome, and roentgenological evidence of increased intracranial pressure. A computed tomography scan and magnetic resonance image showed a huge tumor in the right parietooccipital region. The tumor was totally resected with the involved right transverse sinus in staged operations. Histology was transitional meningioma. The incidence of intracranial meningiomas is low in childhood. The literature is reviewed, and some peculiarities of childhood meningiomas are discussed.

Visual loss and intoxication

The Foster Kennedy Syndrome is very uncommon. The literature cited is often confusing. This paper presents a lucid definition of the syndrome that has contemporary diagnostic value and tenacious historical roots. We attempt to “sort-out” the true Foster Kennedy syndrome from its congeners and discuss the misnomers involved. An illustrative case is presented.

Foster Kennedy syndrome.

Among the syndromes to which the student of neurology is quite early exposed is the Foster Kennedy syndrome or sign. Agreement as to what constitutes the actual syndrome and what are the common causes of it does not exist; therefore, we felt a historical review of the syndrome, including a definition, was pertinent. Prior to a discussion of the syndrome, we review the life of Robert Foster Kennedy, MD. PERSONAL HISTORY Robert Foster Kennedy (Figure) was born in Belfast, Ireland, on Feb 7, 1884. His grandfather was a professor at the Royal University of Ireland, Belfast. One of his cousins was Field Marshall Sir John Dill. Foster Kennedy, as he preferred to be called, graduated from Queens College, Belfast, and received his MD from the Royal University of Ireland in 1906. Shortly after receiving his MD, he was appointed resident house officer at the National Hospital for Nervous Diseases, Queens

Foster-kennedy syndrome due to optochiasmatic arachnoiditis

A case of optochiasmatic arachnoiditis mimicking Foster-Kennedy syndrome is reported. The difficulties in establishing diagnosis are considered, and the literature of optochiasmatic arachnoiditis presenting in this unusual manner is reviewed.

Foster-Kennedy syndrome caused by solitary intracranial plasmacytoma

The first case of typical Foster-Kennedy syndrome, including decreased olfaction of the side of the optic atrophy due to a primary solitary intracranial extraskeletal plasmacytoma, is reported. Its appearance on a computed tomography scan was compatible with a meningioma or subdural hematoma. The patient demonstrated a chronic, corticosteroid-sensitive, relapsing optic neuropathy associated with an elevated sedimentation rate and a monoclonal gammopathy. The diagnosis, treatment, and prognosis of such tumors are reviewed.

Clinical and Computed Tomographic Findings in the Foster Kennedy Syndrome

A 52-year-old man had progressive loss of visual acuity in his left eye associated with anosmia of five years duration. Clinical findings included papilledema in the right eye and optic atrophy in the left eye. A diagnosis of Foster Kennedy syndrome was made. Careful attention to the ophthalmoscopic appearance of the left eye disclosed optic disk swelling in regions without significant atrophy as well as dilated retinal veins. Both of these signs suggested increased intracranial pressure, rather than a primary anterior ischemic optic neuropathy. High resolution computed tomographic scanning confirmed the presence of a large subfrontal meningioma and an expanded right optic nerve sheath, consistent with the papilledema noted clinically.

Giant cell (temporal) arteritis. The differential diagnosis

A patient was referred to the neuro-ophthalmology unit with a diagnosis of Foster-Kennedy syndrome; “papilledema” had been noted in the right eye and optic atrophy in the left. Results of radiographic examinations and lumbar puncture had been normal. The considerations and procedures leading to a correct diagnosis of giant cell arteritis are discussed.

Non-tumor causes of the Foster Kennedy syndrome.

Non-tumor causes of the Foster Kennedy syndrome.

The Foster Kennedy syndrome an evaluation of its diagnostic value.

The Foster Kennedy syndrome an evaluation of its diagnostic value.

Tashima's Syndrome

To the Editor:— This communication describes a new syndrome, which has never been previously reported in the medical literature. It is called Tashima's syndrome and in its full-blown state (forme fruste manifestations may be described in the future) is defined as a condition in which a physician searches for a new sign, disease, or syndrome to which his name can be attached. In this case it is named after the physician who first described the condition, rather than after the patient with the disease, as was the case with de Musset's sign and Christmas disease. Needless to say, confusion as to whether the eponym applies to patient or physician may arise in the assignment of priority when the patient and the doctor both possess the same name. It is still usually possible to assign the proper designation by using the full name. Weir Mitchell's disease and Foster Kennedy syndrome are

Changes of the Optic Nerve after Cataract Extraction Simulating the Foster Kennedy Syndrome

Changes of the Optic Nerve after Cataract Extraction Simulating the Foster Kennedy Syndrome

Foster Kennedy syndrome produced by myelomatous deposits in the skull.

Foster Kennedy syndrome produced by myelomatous deposits in the skull.

Pseudotumoral hypertensive encephalopathy

Some cases of malignant arterial hypertension are reported as pseudotumoral hypertensive with a clinical picture of elevated intracranial pressure, sometimes associated with localizing symptoms, simulating brain tumor. Pseudotumoral hypertensive encephalopathy is relatively frequent in malignant arterial hypertension. It can also be provoked by other disturbances causing arterial hypertension (hormonal, renal, vascular, etc). Some cases of hypertensive encephalopathy are reported. The focal symptoms (Foster-Kennedy syndrome, signs of the posterior fossa, etc.) have been increasing difficulties. The importance of cerebral arteriography and pneumoencephalography is stressed in most of cases avoiding erroneous diagnosis.