Case Report

Dense posterior cerebral artery sign as an acute stroke marker: how to accurately diagnose it in the appropriate setting

Abstract

In recent years, the notion of the hyperdense posterior cerebral artery sign has been put forward as an early marker of acute stroke and a prognostic marker. Although much less frequent than a dense Middle cerebral artery sign, it is important to recognize such a sign especially when accompanying symptoms are present and potential revascu- larization is feasible. We present a case of a hyperdense posterior cerebral artery sign with resulting ischemic involvement of the posterior cerebral artery territory. We will discuss potential pitfall imaging with ways of reducing false-positive and false-negative interpretation when appro- priate symptomatology is present.

Posterior cerebral artery (PCA) strokes represent 5% to 10% of all cerebral infarcts and are associated with a low mortality rate. Patients are usually left with chronic visual, sensory, and motor deficits [1]. Imaging, particularly none- nhanced contrast computed tomography (NECT), plays a pivotal role when evaluating stroke patients in the acute setting with early diagnosis important for further manage- ment. A potentially useful finding is that of the dense artery sign [2-3]. The dense middle cerebral artery (MCA) sign is widely accepted as one of the early imaging features of acute stroke. In the recent years, the notion of the hyperdense PCA sign (HPCAS) has been put forward as an early marker of acute stroke and a prognostic marker. Although much less frequent than a dense MCA sign, it is important to recognize such a sign especially when accompanying symptoms are present and potential revascularization is feasible. We present a case of a HPCAS resulting in ischemic transformation in the PCA territory. We will also discuss potential pitfall imaging with ways of reducing false-positive and false-negative interpretation when appropriate symptomatology is present. A 73-year-old right-handed woman presented with decreased level of consciousness and confusion 2 days after a prosthetic knee replacement surgery. Nonenhanced contrast computed tomography with a thin slice protocol (GE Lightspeed-4 manufactured in Milwaukee, Wis) performed 2 hours after onset of symptoms demonstrated a

left HPCAS within the ambient cistern, initially interpreted as a vascular calcification. (Fig. 1A, B). Subtle loss of gray and white matter differentiation of the medial and inferior temporal and left parahippocampal cortex could be appre- ciated. (Fig. 1B). Two days later, the patient developed moderate right hemiparesis, and right homonymous hemi- anopsia was clinically evident. At that time, the NECT (Fig. 2A, B) showed a definite ischemic infarct involving the hippocampal body and left inferomedial temporal lobe extending into the adjacent posterior internal capsule in proximity to left thalamus with this latter finding explaining the patient hemiparesis (Fig. 2B). The dense PCA sign was not present. The patient evolved favorably with Complete recovery from her hemiparesis but had residual right homonymous hemianopsia.

Approximately 10% to 25% of cerebral infarcts occur in the PCA territory [4], most frequently from proximal atherosclerotic extracranial vertebral arteries embolism or cardioembolism. Nonenhanced contrast computed tomogra- phy scans are routinely performed as the initial diagnostic imaging technique to evaluate known or suspected clinical stroke. The dense artery sign, one of the earliest signs of Acute arterial occlusion, represents either in situ athero- thrombosis or a thromboembolic clot that may or may not be calcified [6]. Some have postulated that the hyperdense sign does not represent the clot itself and results from slow flow, but this is still controversial. Thrombus/emboli within a segment of the PCA is more dense than surrounding structures and has been termed the HPCAS in reference to the more common and frequent dense MCA sign [7]. The HPCAS is defined as a PCA denser than the contralateral counterpart and denser than other visualized vessel of similar size [5-8]. When a PCA stroke is suspected, care must be taken to reduce false-positive and false-negative imaging interpretations especially when appropriate corresponding symptomatology is present such as visual deficits (complete hemianopsia), which is the most common presenting symptom seen in up to 95% of patients, hemisensensory deficits that are usually transient (40%), headache (50%), and alterations in consciousness [5].

Potential false-positive might include [9] atherosclerotic vascular calcification simulating a local thrombus. Vascular calcifications are often bilateral and denser than thrombus, although the size of the vessel and the curved course of the PCA can lead to signal attenuation of these calcifications

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Fig. 1 A-B, NECT demonstrates a dense structure within the ambient cistern in the pathway of the P2-segment HPCAS (white arrow). B, Very subtle loss of gray and white matter differentiation of the medial and inferior temporal and left parahippocampal cortex.

making differentiation with a thrombus/emboli more diffi- cult. Comparison with prior examinations might reveal the presence of such calcifications and limit false-positive interpretations especially in patients with atherosclerotic disease. If the dense sign persists on follow-up examinations, it might suggest a Hypercoagulable state, or a mineralized clot [10].

Fig. 2 A-B, NECT, 2 days after initial computed tomography, showed a definite ischemic infarct involving the hippocampal body and left inferomedial temporal lobe extending into the adjacent posterior arm of the internal capsule (white arrow) in proximity to left thalamus with this latter finding explaining the patient hemiparesis (B).

An other potential situation that can mimic HPCAS include patients with elevated hematocrit in conditions such as polycythemia vera, dehydration, and pulmonary condi- tions (chronic obstructive pulmonary disease) associated with hypoxia secondary to increased levels of erythropoi- etin. A clue to elevated hematocrit being responsible for

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HPCAS is noticing increased density within the rest of the intracranial vessels.

Finally, cerebral edema can give the impression of HPCAS because of a decrease in density of adjacent brain parenchyma simulating increase density within the adjacent vessel. Potential false negative can occur because of anatomic and technical reasons.

The PCA is the main Blood supply to the uppermost midbrain, thalamus, occipital lobes, and the medial and inferior temporal and parietal lobes. The pars circularis (name given because of the circular course of the P1 and P2 segments), which comprise the P1 and P2 segment, ends in the quadrigeminal cistern with the branch of the lateral occipital artery. The HPCAS is usually visualized within the P2 segment in the ambient cistern. The reason is 2-fold: (1) the P2 segment runs horizontally and parallel to the cutting plane; (2) the ambient cistern, which is cerebrospinal fluid filled, allows for adequate contrast with the hyperdense artery. Therefore, in patients with small cisternal spaces (ie, limited cerebral atrophy), the HPCAS might be overlooked. Also, if slices are thicker than the affected vessel, or not parallel to the curved course of the P2 segment within the ambient cistern, the hyperdense artery will not be visualized. Therefore, we recommend performing in all suspected acute thrombus cases, thin-section NECT images rather than 5-mm slice thickness.

In the only study looking specifically at the dense PCA sign [4], 35% of patients (17/48) with PCA infarction had a HPCAS. Complete hemianopia and alterations in conscious- ness were more frequent if the HPCAS was present (P = .009 and P = .002, respectively). The outcome is variable, with some studies demonstrating persistent visual deficit in 84%, sensory deficits in 17%, and motor deficits in 6% of patients [1]. Our patient presented with alterations of consciousness that evolved favorably with complete recovery from her hemiparesis but had residual right homonymous hemianop- sia, which is concordant with the evolution of most patient with a HPCAS.

A HPCAS when combined with acute onset of visual deficits and/or alteration of consciousness is suggestive of early ischemic stroke. Awareness and early identification of a HPCAS can lead to appropriate management with revascularization and potential improvement of patient outcome. Awareness of potential false-positive and false-

negative imaging findings will further permit appropriate imaging diagnosis.

Yves Benabu MD Carolyne Laplante MD

Departement of Diagnostic Radiology

Universite Laval Quebec, Canada

Christian Berthelot MD

Centre Hospitalier affilie universitaire de Quebec

Hopital de l’enfant Jesus

Universite Laval Quebec, Canada

doi:10.1016/j.ajem.2009.12.018

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