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INTRODUCTION

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Orbital disease usually arises within the bony confines of the orbit or by spread from adjacent structures, particularly the paranasal sinuses. The etiology may be inflammation, infection, neoplasia, or vascular anomaly. An orbital mass may also be a metastatic tumor and hence a harbinger of a serious and sometimes life-threatening entity.

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PHYSIOLOGY OF SYMPTOMS

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An increase in orbital volume results in displacement of the globe. Since the orbit has rigid bony walls (see Chapter 1), such displacement usually manifests predominantly as forward protrusion of the globe (proptosis), which is a hallmark of orbital disease. Pathology within the muscle cone displaces the globe anteriorly (axial proptosis). Pathology outside the muscle cone also causes vertical and/or lateral displacement (nonaxial proptosis). Bilateral involvement generally indicates systemic disease, such as autoimmune hyperthyroidism (Graves’ disease). The proptosis in Graves’ ophthalmopathy is often termed exophthalmos.

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Pulsating proptosis may be due to carotid-cavernous fistula, arterial orbital vascular malformation, or transmission of cerebral pulsations due to a bone defect such as in the sphenoid dysplasia of type 1 neurofibromatosis. Proptosis that increases on bending the head forward or with Valsalva maneuver can be a sign of venous orbital vascular malformation (orbital varices) or bone defect. Intermittent proptosis may be the result of a sinus mucocele. The Hertel exophthalmometer (see Chapter 2) is the standard method of quantifying the magnitude of proptosis. Serial measurements are most accurate if performed by the same individual with the same instrument. Pseudoproptosis is apparent proptosis in the absence of orbital disease. It may be due to an enlarged globe from high myopia or buphthalmos, lid retraction, extraocular muscle weakness or paralysis, asymmetrical orbital size, or posterior displacement (enophthalmos) of the contralateral globe.

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Proptosis does not impair vision unless there are corneal changes due to corneal exposure. However, any orbital process that arises from, involves, or compresses the optic nerve, can result in an optic neuropathy that may manifest as a relative afferent pupillary defect or reduction of color vision before there is reduction of visual acuity. In addition, visual impairment may be caused by compression of the globe resulting in distortion of the retina and possible elevation of intraocular pressure.

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Limitation of ocular movements resulting in binocular diplopia (double vision) may be due to direct involvement of the extraocular muscles, interference with their mechanisms of action, or dysfunction of the third (oculomotor), fourth (trochlear), or sixth (abducens) cranial nerves. Pain may occur as a result of rapid expansion or inflammation or the orbital tissues or infiltration of sensory nerves.

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Disease involving the superior orbital fissure produces a characteristic combination (superior orbital fissure syndrome) of diplopia (third, fourth, and/or sixth cranial nerves), corneal and facial anesthesia (first [ophthalmic] division of fifth [trigeminal] cranial nerve), and possible proptosis. Disease at the orbital apex also causes visual ...

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