Computed Tomography in Cerebrovascular Disease Ramon Berguer Noncontrast computed tomography (CT) and CT angiography are the gold standards today to select symptomatic patients for surgical or interventional therapies of the carotid or vertebral arteries. Present day multisection CT machines are an improvement over older single-section spiral CT and can acquire the needed information about the arteries of the neck and brain in 20 seconds. This improvement in efficiency is most relevant to the early initiation of treatment for acute strokes. The traditional coupling of the concepts of brain infarction and clinical stroke was put into question by the general use of CT. Clearly, brain infarction can occur without a stroke, and what is labeled clinically as a transient ischemic attack (TIA) may be the result of a brain infarction. The incidence of silent infarction (17%) in asymptomatic patients with carotid bifurcation disease and the high probability of infarction (40%) in patients with history of a TIA suggest that a noncontrast CT should precede any inclusion of a patient in randomized studies that attempt to compare one intervention to another. No study protocol should attempt to grade the morbidity of a procedure, such as carotid stenting, by adding a CT to the clinical follow-up if it does not include the status of the brain at the time of recruitment. Although TIAs are cognitively associated with a temporary and reversible perfusion defect, actually up to 30% of patients with a TIA have an appropriate infarct seen on CT. If the patient who has a TIA is also known to have a carotid stenosis, in 45% of cases an infarct is seen that can be presumed to have been the cause of the TIA. The workup of patients with hemispheric TIA should include CT angiography to define both the causative lesion and other concomitant lesions, such as plaques in the siphon, unexpected internal carotid dissection, and proximal lesions in the innominate or common carotid arteries. The CTA will also document the location and size of existing brain infarcts. Although CT is the best tool for imaging diagnostics in the carotid system, its usefulness in the vertebrobasilar territory is limited. CT angiography might not reveal certain cerebellar infarcts and most of the minute pontine infarcts that result from occlusion of the small perforating arteries of the pons in patients with TIAs or strokes of vertebrobasilar distribution. The diminished optical resolution of CT in the brain stem derives from the dense bone that surrounds it causing refraction artifacts. Parenchymatous changes in the vertebrobasilar territory are better demonstrated with magnetic resonance imaging (MRI). Although multidetector CT angiography can scan the entire vertebrobasilar system in 30 seconds, the limited access to the patient’s neck while maintaining the head in the trigger position makes it an impractical alternative to dynamic arteriography for the diagnosis of vertebrobasilar ischemia secondary to rotation and extension of the neck (bow-hunter syndrome). In patients who have had a stroke, CT angiography using nonionic intravenous contrast is indicated upon admission. The diagnostic value of CT has a time scale. The CT does not show large cortical infarcts for the first 3 hours; however, by 24 hours, approximately 60% of infarcts are seen, and at 7 days 100% become evident. Even when the infarct is not visible yet, a CT angiogram obtained within the first hours after a stroke corresponding to an infarction in the middle cerebral artery territory can display indirect signs that predict the location and extent of the infarction. These signs are the obscuration of the lentiform nucleus and the loss of the insular ribbon. The lentiform nucleus is perfused by the lenticulostriate branches of the middle cerebral arteries. These are practically terminal arteries that cannot be resupplied by collateral flow. Their lack of perfusion causes edema that obscures the silhouette of the lentiform nucleus. The insular ribbon is the white–gray matter contrast that forms the lateral margin of the insula. The insula, like the lentiform nucleus, is far from the collateral supply that could be derived from the anterior or posterior cerebral arteries. Here too, edema blurs the contrast between white and gray matter. Large hemispheric or cerebellar infarcts produce mass effects (from edema) that result in the effacement of the sulci and of the lateral ventricle. In general, early CT signs of a large infarction contraindicate an intervention because intervention could result in a more ominous hemorrhagic infarction of the ischemic brain. In patients with a past history of stroke, the CT angiogram identifies the causative lesion and assesses what brain remains at risk. Traditionally, immediate noncontrast CT has been advocated in a patient who develops an acute stroke after an operation in order to rule out a hemorrhagic infarction. In the setting of a postoperative endarterectomy, the finding of a hemorrhagic infarction would be extraordinary. The author has never observed such. If a patient wakes up intact from anesthesia and 15 to 30 minutes later develops a neurologic deficit, the cause is usually red or gray thrombus at the endarterectomy site. Obtaining a CT in these circumstances to exclude possible hemorrhagic infarction will delay the necessary urgent reexploration of the endarterectomy and probably negate the opportunity for reversing the neurologic deficit. CT angiography is routinely used in the evaluation of carotid and vertebral artery dissections. In carotid and vertebral artery dissections, MRI traditionally has been used for diagnostic and follow-up evaluations. Although MRI is superior in outlining parenchymatous changes, CT is superior in terms of outlining the arterial source (e.g., flap, luminal narrowing, wall hematoma, false aneurysm).
Computed Tomography in Cerebrovascular Disease Ramon Berguer Noncontrast computed tomography (CT) and CT angiography are the gold standards today to select symptomatic patients for surgical or interventional therapies of the carotid or vertebral arteries. Present day multisection CT machines are an improvement over older single-section spiral CT and can acquire the needed information about the arteries of the neck and brain in 20 seconds. This improvement in efficiency is most relevant to the early initiation of treatment for acute strokes. The traditional coupling of the concepts of brain infarction and clinical stroke was put into question by the general use of CT. Clearly, brain infarction can occur without a stroke, and what is labeled clinically as a transient ischemic attack (TIA) may be the result of a brain infarction. The incidence of silent infarction (17%) in asymptomatic patients with carotid bifurcation disease and the high probability of infarction (40%) in patients with history of a TIA suggest that a noncontrast CT should precede any inclusion of a patient in randomized studies that attempt to compare one intervention to another. No study protocol should attempt to grade the morbidity of a procedure, such as carotid stenting, by adding a CT to the clinical follow-up if it does not include the status of the brain at the time of recruitment. Although TIAs are cognitively associated with a temporary and reversible perfusion defect, actually up to 30% of patients with a TIA have an appropriate infarct seen on CT. If the patient who has a TIA is also known to have a carotid stenosis, in 45% of cases an infarct is seen that can be presumed to have been the cause of the TIA. The workup of patients with hemispheric TIA should include CT angiography to define both the causative lesion and other concomitant lesions, such as plaques in the siphon, unexpected internal carotid dissection, and proximal lesions in the innominate or common carotid arteries. The CTA will also document the location and size of existing brain infarcts. Although CT is the best tool for imaging diagnostics in the carotid system, its usefulness in the vertebrobasilar territory is limited. CT angiography might not reveal certain cerebellar infarcts and most of the minute pontine infarcts that result from occlusion of the small perforating arteries of the pons in patients with TIAs or strokes of vertebrobasilar distribution. The diminished optical resolution of CT in the brain stem derives from the dense bone that surrounds it causing refraction artifacts. Parenchymatous changes in the vertebrobasilar territory are better demonstrated with magnetic resonance imaging (MRI). Although multidetector CT angiography can scan the entire vertebrobasilar system in 30 seconds, the limited access to the patient’s neck while maintaining the head in the trigger position makes it an impractical alternative to dynamic arteriography for the diagnosis of vertebrobasilar ischemia secondary to rotation and extension of the neck (bow-hunter syndrome). In patients who have had a stroke, CT angiography using nonionic intravenous contrast is indicated upon admission. The diagnostic value of CT has a time scale. The CT does not show large cortical infarcts for the first 3 hours; however, by 24 hours, approximately 60% of infarcts are seen, and at 7 days 100% become evident. Even when the infarct is not visible yet, a CT angiogram obtained within the first hours after a stroke corresponding to an infarction in the middle cerebral artery territory can display indirect signs that predict the location and extent of the infarction. These signs are the obscuration of the lentiform nucleus and the loss of the insular ribbon. The lentiform nucleus is perfused by the lenticulostriate branches of the middle cerebral arteries. These are practically terminal arteries that cannot be resupplied by collateral flow. Their lack of perfusion causes edema that obscures the silhouette of the lentiform nucleus. The insular ribbon is the white–gray matter contrast that forms the lateral margin of the insula. The insula, like the lentiform nucleus, is far from the collateral supply that could be derived from the anterior or posterior cerebral arteries. Here too, edema blurs the contrast between white and gray matter. Large hemispheric or cerebellar infarcts produce mass effects (from edema) that result in the effacement of the sulci and of the lateral ventricle. In general, early CT signs of a large infarction contraindicate an intervention because intervention could result in a more ominous hemorrhagic infarction of the ischemic brain. In patients with a past history of stroke, the CT angiogram identifies the causative lesion and assesses what brain remains at risk. Traditionally, immediate noncontrast CT has been advocated in a patient who develops an acute stroke after an operation in order to rule out a hemorrhagic infarction. In the setting of a postoperative endarterectomy, the finding of a hemorrhagic infarction would be extraordinary. The author has never observed such. If a patient wakes up intact from anesthesia and 15 to 30 minutes later develops a neurologic deficit, the cause is usually red or gray thrombus at the endarterectomy site. Obtaining a CT in these circumstances to exclude possible hemorrhagic infarction will delay the necessary urgent reexploration of the endarterectomy and probably negate the opportunity for reversing the neurologic deficit. CT angiography is routinely used in the evaluation of carotid and vertebral artery dissections. In carotid and vertebral artery dissections, MRI traditionally has been used for diagnostic and follow-up evaluations. Although MRI is superior in outlining parenchymatous changes, CT is superior in terms of outlining the arterial source (e.g., flap, luminal narrowing, wall hematoma, false aneurysm).
