72Chapter 4: Radiographic errors

reversal of flow through the ophthalmic artery, and permanent visual loss is distinctly uncommon. On the other hand, the incidence of stroke associated with carotid dissection is high, ranging from 12 to 40%. The risk of stroke is highest in the initial two weeks following dissection and diminishes considerably thereafter. If a patient is seen during this time, anticoagulation should be considered, initially with heparin and then with warfarin. Patients who are evaluated one month or more after the acute event can usually be treated with anti-platelet agents alone.

Traumatic dissections are usually due to severe blunt head or neck injury such as motor vehicle accidents, fistfights, hanging, surgery or manipulative neck therapy. Many cases of so-called “spontaneous” dissection may actually have a traumatic origin as well, though the precipitating event may seem trivial, such as coughing, sneezing, childbirth, athletic activities, painting a ceiling, carrying a heavy load or riding a roller coaster. Some patients with spontaneous dissection have an identifiable predisposing disorder such as fibromuscular dysplasia, Marfan’s syndrome, Ehlers–Danlos syndrome, alpha-1 antitrypsin deficiency, cystic medical necrosis, syphilis or vasculitis.

Most cases of dissection can be diagnosed with non-invasive methods, including MRI, MR angiography (MRA), CT angiography (CTA) and carotid Dopplers. The study of choice is an axial T1or T2weighted pre-contrast MRI of the head that includes images down to the carotid bifurcation. On such images, dissection appears as a bright crescentshaped signal around the ICA due to the hyperintense signal of methemoglobin within the vessel wall. Significant narrowing of the lumen, when present, is better documented with MRA or by conventional angiography, and appears as the “string sign”. Because angiographic methods (whether by catheter study, MRA or CTA) visualize blood flow, dissections that do not impinge on the lumen may not be demonstrable with these techniques but are better identified with MR images, as illustrated by the above case.

Diagnosis: Internal carotid artery dissection

Tip: An acute, postganglionic Horner syndrome with persistent pain is usually due to internal carotid artery dissection. Careful inspection of axial T1or T2-weighted MR images will reveal the characteristic bright crescent around the artery.

Headache and bilateral third nerve palsy

Case: This 38-year-old, previously healthy maintenance man presented to the emergency room because of chest pain, for which he received tissue thromboplastin activator. The following day he experienced severe headache, photophobia and diplopia. Neurologic examination showed bilateral third nerve palsies, more severe on the right side, and a CT scan was read as normal (Figure 4.12).

What is the diagnosis? What confirmative study would you order?

The abrupt onset of headache and bilateral third nerve palsy is strongly suggestive of pituitary apoplexy, particularly following the use of a thrombolytic agent. This patient’s facial features (prominent chin and brow) are characteristic of acromegaly and suggest the presence of a longstanding pituitary tumor. An MRI was obtained, confirming a suprasellar mass with cavernous sinus invasion and hemorrhage (Figure 4.13). In retrospect, his previous CT scan also showed soft tissue in the suprasellar cistern that had been overlooked. Endocrine evaluation showed pituitary insufficiency and elevated growth hormone levels. He was treated with steroids and underwent transphenoidal subtotal resection of his pituitary tumor. Follow-up three months later showed partial recovery of third nerve function.

Discussion: Hemorrhage or infarction of the pituitary gland, usually due to an underlying tumor, is termed pituitary apoplexy. This condition typically affects adults and has a wide range of clinical

presentations. Most patients experience abrupt onset of severe headache with symptoms and signs related to meningeal irritation. Some patients also exhibit altered mental status, cranial neuropathy and visual loss due to chiasmal compression. The presence of nuchal rigidity, photophobia and reduced level of consciousness in some patients with this condition may be mistakenly attributed to an aneurysmal subarachnoid hemorrhage or infectious meningitis. Visual loss may be unilateral or bilateral with variable severity. Clouding of consciousness may preclude detailed visual testing; when such testing is possible, a bitemporal pattern of loss is characteristic. Ophthalmoplegia, due to compression of the ocular motor nerves in the cavernous sinus, is also common and may also be uni-

lateral or bilateral. The third nerve is most commonly affected, followed by the sixth and fourth cranial nerves. The advent of high-resolution MR scanning now allows the detection of hemorrhage into a pituitary tumor in occasional patients who have minimal or no symptoms. Strictly speaking, such patients can be classified as having pituitary apoplexy although some authors reserve the term apoplexy for those with a dramatic clinical presentation as described above.

In the majority of cases of apoplexy, the presence of a pituitary tumor was unsuspected prior to hemorrhage. In approximately one-third of patients some sort of precipitating factor is identified. These precipitating events are quite varied, including reduced blood flow to the pituitary gland (as

Figure 4.13 MRI of the above patient. Coronal non-contrast T1-weighted image reveals a sellar mass extending into the suprasellar cistern, just contacting but not compressing the optic chiasm. Heterogeneous signal intensity within the mass is consistent with hemorrhage from pituitary apoplexy. The mass extends into the cavernous sinuses, more pronounced on the right side (arrow) (courtesy of Dr. Bradley Robottom).

from hypotension or Valsalva maneuver), an acute increase in blood flow (as in malignant hypertension), stimulation of the pituitary gland (such as pregnancy or with exogenous estrogen administration), emboli from carotid artery surgery, and coagulopathy (from thrombocytopenia, administration of anticoagulant drugs, and thrombolytic agents as in the case under discussion). The occurrence of sudden headache and visual symptoms (afferent and/or efferent) in any of these settings should suggest the possibility of pituitary apoplexy. Because of its varied clinical presentations and at times ambiguous or subtle radiographic findings, a delayed diagnosis of pituitary apoplexy is not uncommon.

Although a standard head CT is usually the most easily accessed radiographic study in an emergency room setting, this imaging study is less effective than MRI for the detection of pituitary apoplexy. CT

Figure 4.14 CT scan of another patient with pituitary apoplexy causing severe headache, acute bilateral visual loss and ophthalmoplegia. Note the distortion of the suprasellar cistern anteriorly, which is due to filling of this CSF space by infarcted pituitary tissue (arrow).

is often degraded at bone to soft tissue interfaces and is thus less sensitive for visualizing lesions at the skull base. In addition, the suprasellar cistern is a midline structure and therefore detection of an abnormality depends on the examiner’s familiarity with its normal appearance. On CT the suprasellar cistern appears as a low density five-sided hypodense area anterior to the midbrain. In many cases the presence of a tumor is manifest not as a visible mass, but as filling in of this CSF-filled space (Figure 4.14). MRI, in contrast, is much better suited for the detection of tumors in this region, and is thus the study of choice in cases of suspected pituitary apoplexy.

Prompt diagnosis of pituitary apoplexy is crucial because these patients are at risk for the systemic complications of acute adrenal insufficiency. Acute management should include the administration of systemic corticosteroids in stress dosages (e.g.