The Royal College of Radiologists of the United Kingdom affirm that CT is the optimal investigation for orbital pathology because of the good spatial resolution and inherent contrast of soft tissues with orbital fat. Diseases affecting the orbit are considered according to the anatomical compartment in which they originate; intraconal: within the muscle cone; conal: involving the muscle cone; and extraconal: outwith the muscle cone, e.g. sinus, bone, lachrymal gland. In general, extraconal pathology produces globe proptosis with an early presentation with diplopia. Intraconal or conal lesions produce proptosis with restricted eye movement. Diplopia without proptosis indicates retro-orbital or midbrain pathology (see Chapter 6). Globe disease is well assessed by clinical visual inspection and ultrasound, rarely is CT necessary.

Thin section helical scanning is best; IV contrast is not necessary in primary screening as most orbital masses enhance to the same extent as the muscles so, therefore, there is no differential enhancement to assist in making a tissue specific diagnosis. If there is a history of pulsatile exophthalmos then a MDCT angiogram (MDCTA) protocol is required. As with most neurological disease, it is necessary to have an accurate history and examination to enable CT to provide an optimal examination.

The orbit links onto other important skull base areas and pathology in these areas overlaps clinically; therefore, illustrations may overlap with those in other chapters including visual failure, pituitary, and the cavernous sinus.

Patient preparation is described in Table 3.1 and a surview in figure 3.1A.

The images can be presented in the axial, coronal, and sagittal planes if required. The multiplanar reformats can be done with 2 mm slice width/2 mm interspace to show all structures clearly (3.1B), with the axials angled along the optic nerves in a line taken from the posterior clinoid through the globe (3.1C). MPR curved planes are occasionally useful. Protocol parameters are presented in Table 3.2.