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Clinical Neuroanatomy
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Involvement of the optic nerve immediately behind the optic foramen can produce bilateral visual problems. The inferior nasal fibres of the opposite optic nerve not only cross in the chiasm but also sweep forwards into the optic nerve before turning sharply to head posteriorly into the chiasm and optic tract. They can therefore be damaged by a lesion just anterior to the chiasm. A meningioma of the tuberculum sellae is the most likely lesion to be found at this site. This can produce a blind eye, an upper temporal field defect in the contralateral eye (called a junctional scotoma) and, if large, may cause loss of smell on the same side as the blind eye and eventually papilloedema in the opposite eye, the swelling in the blind eye being prevented by the compressing lesion. This constitutes the well known, but extremely rare, Foster–Kennedy syndrome.
Abnormalities of Smell
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Richard L. Doty, Steven M. Bromley
A number of tumours in and around the olfactory bulbs or tracts can cause olfactory disturbance. Examples include olfactory groove meningiomas, frontal lobe gliomas, and suprasellar ridge meningiomas arising from the dura of the cribriform plate. Due to the olfactory nerve’s close location to the roof and medial wall of the orbit, as well as the optic nerves and tracts, structural lesions affecting smell may also affect vision. Also, olfactory tumours may extend into the frontal lobes resulting in symptoms of dementia and possibly the release of primitive reflexes (e.g., grasping, snout, and glabellar). Mass lesions need not be in the olfactory tracts to cause smell impairment. Ishimaru and colleagues44 identified two patients with hyposmia from tumours to the right frontal lobe; the hyposmia reversed with craniotomy and tumour resection. Mass lesions around the olfactory region can result in a Foster-Kennedy syndrome, which consists of: (a) ipsilateral anosmia, (b) ipsilateral optic atrophy, and (c) contralateral papilledema secondary to raised intra-cranial pressure.45Pseudo Foster-Kennedy syndrome has been reported in patients with increased intra-cranial pressure who had previous unilateral optic atrophy.46 Similarly, tumours in central regions of olfactory processing (e.g., mesial temporal lobe) can also potentially affect smell. Headache often accompanies a complaint of smell loss when the aetiology is a mass lesion. Lymphoma has been known to infiltrate into olfactory areas and cause dysfunction. Similarly, granulomatous diseases – such as syphilis, sarcoidosis, SLE, and Wegener’s granulomatosis – often result in anosmia. In patients suspected of having a neoplasm, neuroimaging is essential.
Unilateral Vision Loss as the Only Presenting Symptom of Type 2 Foster Kennedy Syndrome
Published in Neuro-Ophthalmology, 2023
Husayn Gulamhusein, Amadeo R. Rodriguez
Foster Kennedy syndrome is a well-known neuro-ophthalmological entity owing to its elegant pathophysiology: direct ipsilateral tumour compression with axonal loss that precludes the occurrence of papilloedema, whereas the contralateral optic nerve, also exposed to raised intracranial pressure but with viable axons, becomes oedematous. However, this syndrome is seldom encountered in practice. In 1967, von Wowern reported an incidence ranging from 0.9% to 2.5% of intracranial lesions.1 It is reasonable to assume that nowadays its frequency is even lower due to improved healthcare access and advances in neuroimaging. This typical presentation is sometimes described as type 1, to differentiate it from two other possible forms of the syndrome which are less well recognised, but also included in Foster Kennedy’s original paper.2 These other forms are bilateral optic disc oedema eventually evolving into unilateral optic atrophy (type 2), and bilateral optic disc oedema with subsequent development of bilateral optic atrophy (type 3).3,4 This combination of findings can be produced by anterior fossa lesions such as frontal tumours and olfactory groove or sphenoid wing meningiomas.5