BACKGROUND: Transcranial Doppler sonography (TCD) is a noninvasive method for detecting arterial cerebral vasospasm (CVS) in aneurysmal subarachnoid hemorrhage (SAH). Computed tomographic angiography (CTA) has been increasingly used for CVS diagnosis. The purpose of this study was to evaluate the degree of agreement between TCD and CTA in diagnosing clinical CVS following SAH, and to define the role of CTA in triaging patients prior to digital subtraction angiography (DSA) and endovascular intervention. METHODS: Fifty-five consecutive patients with aneurysmal SAH who underwent sequential TCD and CTA were analyzed. TCD CVS was defined as anterior circulation peak mean velocity (PMV) >160 cm/s, basilar artery (BA) PMV >90 cm/s, and Lindegaard ratio (LR) >6. CTA CVS was defined as >50% luminal narrowing in the affected vessel. Clinical CVS was defined as the onset of new focal neurological deficit attributed to delayed ischemic injury. RESULTS: Thirteen patients (24%) had clinical CVS and 42 patients (76%) were asymptomatic. All patients with clinical CVS had also radiological evidence of CVS (agreement 100%). In 35 patients without clinical CVS, both tests agreed for absence of CVS in 28 cases (agreement 83%). The remaining 7 asymptomatic patients had radiological CVS only, in disagreement with clinical absence of CVS (17%). CONCLUSIONS: Clinical evaluation and TCD can reliably diagnose CVS in symptomatic patients and PMV >180 cm/s, or can rule out CVS in asymptomatic patients with PMV <140 cm/s. In this category of patients, adding a CTA to clinical evaluation and TCD may not be warranted.
BACKGROUND: Transcranial Doppler sonography (TCD) is a noninvasive method for detecting arterial cerebral vasospasm (CVS) in aneurysmal subarachnoid hemorrhage (SAH). Computed tomographic angiography (CTA) has been increasingly used for CVS diagnosis. The purpose of this study was to evaluate the degree of agreement between TCD and CTA in diagnosing clinical CVS following SAH, and to define the role of CTA in triaging patients prior to digital subtraction angiography (DSA) and endovascular intervention. METHODS: Fifty-five consecutive patients with aneurysmalSAH who underwent sequential TCD and CTA were analyzed. TCD CVS was defined as anterior circulation peak mean velocity (PMV) >160 cm/s, basilar artery (BA) PMV >90 cm/s, and Lindegaard ratio (LR) >6. CTA CVS was defined as >50% luminal narrowing in the affected vessel. Clinical CVS was defined as the onset of new focal neurological deficit attributed to delayed ischemic injury. RESULTS: Thirteen patients (24%) had clinical CVS and 42 patients (76%) were asymptomatic. All patients with clinical CVS had also radiological evidence of CVS (agreement 100%). In 35 patients without clinical CVS, both tests agreed for absence of CVS in 28 cases (agreement 83%). The remaining 7 asymptomatic patients had radiological CVS only, in disagreement with clinical absence of CVS (17%). CONCLUSIONS: Clinical evaluation and TCD can reliably diagnose CVS in symptomatic patients and PMV >180 cm/s, or can rule out CVS in asymptomatic patients with PMV <140 cm/s. In this category of patients, adding a CTA to clinical evaluation and TCD may not be warranted.
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