dilate as well as the normal pupil then the lesion is a postganglionic one. Attention to other localizing signs and symptoms is important. If brainstem signs are present, an MRI of the brain with contrast is sufficient. If brainstem signs are absent, then a study of the head, neck and chest should be obtained. Preganglionic Horner syndrome due to apical lung tumor is typically accompanied by ipsilateral arm pain due to infiltration of the brachial plexus. Postganglionic Horner syndrome commonly presents as an isolated finding, usually accompanied by ipsilateral head/face pain. In such cases the evaluation should include MR images of the head and neck and MRA with particular attention to the internal carotid artery.

A similar pitfall may occur in the evaluation of increased ICP. Most cases of increased ICP are due to a disease process within the cranial cavity and if the causative lesion is structural an appropriate scan of the head will reveal it. An important exception to this is the patient with a compressive mass in the neck producing obstruction of the venous outflow from the head (Figure 4.10). In such cases the diagnosis may be missed if radiographic studies do not include views of the neck as well as the head.

Diagnosis: Postganglionic Horner syndrome

Tip: Investigation of a postganglionic Horner syndrome should include MR imaging of head and neck in order to visualize the area of the superior cervical ganglion and carotid bifurcation.

Figure 4.10 Axial post-contrast CT of the neck in a different patient with increased intracranial pressure. There are bilateral paragangliomas, right greater than left (arrows), compressing the right jugular vein and producing a secondary pseudotumor syndrome. This is another example of a case in which the diagnosis would be missed if imaging were restricted to the head.

70Chapter 4: Radiographic errors

Subtle radiographic findings

Some radiographic abnormalities are difficult to detect because they are small or subtle. In such cases it is particularly important for the clinician to have a strong suspicion regarding the location and nature of the lesion and to communicate this effectively to the neuroradiologist. In these cases the “trick” to reading the scan is knowing what should be there.

“Boxer” ptosis

Case: A 45-year-old factory worker was “headbutted” by her boxer dog while bending over, striking her on the right cheek and throwing her upward and back. The next day she developed a “black eye” with some local tenderness. The discoloration faded over the next week, but just as it was almost gone she developed moderately severe pain behind the right eye that extended to the temple and vertex. Two days later, right upper lid ptosis was noticed by a co-worker.

Examination showed normal afferent visual function and ocular motility. The right pupil measured 3 mm in dim illumination and 2 mm in bright light, the left 5 mm in dim and 2.5 mm in bright light. Both pupils reacted briskly to light but the right pupil showed a delayed response to dark (dilation lag). There was 2 mm of right upper lid ptosis and mild “reverse” lower lid ptosis (Figure 4.11A). Instillation of hydroxyamphetamine produced 3 mm of pupillary dilation on the left side only. An MR scan of head, neck and orbits was reportedly normal.

The above clinical findings are characteristic of a postganglionic Horner syndrome. How might this be related to her preceding trauma?

When the patient was struck by her dog she was thrown back, causing brief but forceful hyperextension of her neck. This form of neck trauma can produce a shearing injury to the internal carotid artery with subsequent dissection, thus causing damage

to the oculosympathetic fibers. Careful examination of her MRI revealed a hyperintense crescent adjacent to the left internal carotid artery on the axial T2-weighted image, characteristic of dissection (Figure 4.11B). An MRA showed some irregularity of the cervical arteries consistent with fibromuscular dysplasia (Figure 4.11C). This underlying vasculopathy presumably rendered her arteries susceptible to damage from relatively trivial trauma.

Discussion: Most cases of acute, painful, postganglionic Horner syndrome are due to carotid dissection or cluster headache. The non-remitting nature of the pain in dissection should help to distinguish these patients from those with cluster headache. Patients with cluster headache typically experience abrupt episodes of pain, frequently occurring during the night and lasting 45–60 minutes. These painful attacks are often associated with a Horner syndrome, which is usually transient but may become permanent after repeated episodes. In some affected individuals, cluster attacks are precipitated by ingestion of alcohol and, for reasons that remain obscure, sufferers often prefer to pace about during their attacks rather than resting in bed.

In contrast, the pain of internal carotid artery (ICA) dissection is unremitting. Pain, which may be localized to the head, eye, jaw, face or neck, is present in over 90% of patients and may be the only manifestation. Scalp tenderness may occur, suggesting a diagnosis of giant cell arteritis (GCA). A postganglionic Horner syndrome occurs in up to 58% of patients with carotid dissection and can be the presenting manifestation.

Transient monocular blindness is reported by about 30% of patients with ICA dissection and is probably caused by decreased perfusion secondary to reduction of the carotid lumen rather than by retinal emboli. Episodes of transient monocular visual loss due to dissection are often precipitated by postural change and may be associated with positive visual phenomena including sparkles and scintillations. ICA dissection can produce retinal emboli but this is rare, probably because of