FURTHER READING

Neuro-imaging

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R. J. Wolnitz, J. D. Trobe, W. T. Cornblath et al., Common errors in the use of magnetic resonance imaging for neuro-ophthalmic diagnosis. Surv Ophthalmol, 45 (2000), 107–14.

Canalicular meningioma

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S.Lessell, Current concepts in ophthalmology: optic neuropathies. N Eng J Med, 299 (1978), 533–6.

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Cerebral venous thrombosis

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Horner syndrome and carotid dissection

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Pituitary apoplexy

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Chronic sixth nerve palsy

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Certain signs and symptoms are seen frequently as a normal variant in some individuals but may also signify illness in others. An example of this is the decreased sense of smell that may be normal in a long-term smoker but is also a classic symptom of a subfrontal meningioma. Similarly, facial asymmetry may be written off as a normal congenital variant but can also be a subtle sign of mild seventh nerve paresis from a growing brainstem tumor. Deciding when a sign or symptom should be pursued and when it should be ignored is a valuable clinical skill. This is also true when interpreting radiographic findings. Certain scan abnormalities that may occur in some individuals as a normal variant or an incidental finding (sometimes termed an “incidentaloma”) may be a sign of a disease process in others. In this section we look at a few such examples. In each case, it is the responsibility of the clinician to correlate the scan finding with the clinical information in order to appreciate its diagnostic significance. Part of this process should include personally reviewing the scan in the context of the clinical abnormalities, rather than relying on a written radiographic report.

Empty sella

Case: A 36-year-old homemaker sought medical attention because of intermittent horizontal diplopia. She had gained weight following each of her three pregnancies and had a long history of chronic daily headaches but was otherwise healthy.

Figure 5.1 Empty sella. Coronal non-contrast T1-weighted MRI of a 36-year-old homemaker with IIH shows enlargement of the sella turcica and downward flattening of the pituitary gland.

Examination showed mild fullness of the optic discs with normal optic nerve function and normal ocular motility. A brain MRI was unremarkable except for an enlarged and “empty” sella, reported as a normal variant (Figure 5.1). She was treated with a series of medications for muscle contraction headaches and then for migraine without much success. Eventually, a lumbar puncture was performed which demonstrated elevated intracranial pressure (ICP) of 300 mm of water with normal cerebrospinal fluid constituents, leading to a diagnosis of idiopathic intracranial hypertension (IIH).

Discussion: An enlarged sella without associated enlargement of the pituitary gland sometimes occurs following treatment of a pituitary tumor or after pituitary apoplexy and, in this context, is referred to as “secondary” empty sella syndrome. In contrast, patients with this finding and no prior history of pituitary enlargement are said to have “primary” empty sella syndrome. This radiographic finding may occur as a normal variant, reportedly seen in up to 20% of normal individuals, or it may be a sign of long-standing increased ICP.

Although the original definition of IIH stipulates that radiographic studies must be normal, minor abnormalities are in fact commonly seen, particularly on MR rather than CT scans. A study examining the MRI findings in a group of 20 patients with idiopathic intracranial hypertension found that subtle radiographic abnormalities indicative of increased ICP were common in IIH. Flattening of the posterior globe was seen in 80% of patients, an empty sella in 70% and expansion of the perioptic spaces in 45% (Figure 5.2A and B). In addition, papilledema was frequently visible, appearing as enhancement of the prelaminar optic nerve in 50% and as intraocular protrusion of the optic nerve in 30% (Figure 5.2C). A small degree of cerebellar tonsillar descent is also seen in some patients with chronically increased ICP.

Low cerebellar tonsils

Case: A 27-year-old woman with a history of chronic headaches experienced new onset of blurred vision, intermittent horizontal diplopia and occasional paresthesias in her arms and legs. Her examination revealed normal visual function and fundus appearance. She had a comitant esophoria that broke down easily to an esotropia but no ductional deficit and no saccadic slowing. She had a little difficulty with tandem gait and an otherwise normal neurologic examination. Demyelinating disease was suspected and an MR scan was obtained (Figure 5.3). The scan showed no white-matter lesions although the official report did mention mild protrusion of the cerebellar tonsils through the foramen magnum. The patient’s physician noted this on the report but considered it to be an incidental finding. The patient was reassured that there was no sign of multiple sclerosis.

Discussion: A comitant esodeviation without a ductional deficit is most often due to congenital esotropia in children, and to decompensation of a pre-existing esophoria when encountered in adults. Less commonly, comitant esotropia is due to acquired disease, usually related to increased ICP or involving the posterior fossa. Specific causes