As noted above, NCCT has been the preferred modality for initial imaging of suspected stroke because it is widely available and very sensitive for acute hemorrhage. CT effectively detects acute hemorrhage in brain parenchyma and in the subarachnoid, subdural, and intraventricular spaces. Unfortunately, it is insensitive at detecting acute ischemic tissue injury. Recent development of computed tomographic perfusion (CTP) imaging has increased sensitivity for detection of acute cerebrovascular-induced tissue damage. While CTP imaging requires contrast, magnetic resonance perfusion (MRP) imaging may be performed with or without contrast.

CT perfusion studies are performed by rapidly imaging and reimaging a target region of the brain immediately following contrast bolus. The technique is based on the central volume principle which states that CBF is equivalent to the cerebral blood volume (CBV) divided by the mean transit time (MTT). Both CTP and MRP imaging can measure CBV, CBF, time to peak (TTP), and MTT. Quantitative and qualitative measurement of these parameters provides a method of assessing regional tissue perfusion to identify relative regions of ischemia or infarction. In general, a CBF of 10–15 mL/100 g/min or less is considered infarcted tissue whereas a rate of 15–20 mL/100 g/min is considered ischemic. Any region of tissue that is under-perfused, but not infracted, surrounding infracted tissue is considered the penumbra. Alternatively the penumbra can also be considered as a volume of low blood flow tissue that is larger than the infarcted volume by 20 % or more. Relative “mismatch” of tissue flow and volume compared with the centrally infracted core tissue, in the absence of acute hemorrhage, indicates brain tissue that may be salvaged with the use of thrombolytic therapy. Technically, MRP has several advantages over CTP. It does not use ionizing radiation, has less risk of renal toxicity, known contrast reactions, and does not cause fluid overload compared to iodinated contrast materials. MRP has less variability than CTP quantitative methods [44], and, unlike CT, MRI can measure directly cellular viability using diffusion restriction techniques. It also can assess a larger volume of brain tissue than CTP. The newer generation of CT scanners, with their larger number of detector arrays, is decreasing the volume gap between techniques, however [45]. Despite these advantages, the wide availability of CT and the rapidity with which it can be performed in a limited 3 h clinical onset window mitigates the advantages of MR. Given the abovementioned risks and benefits of imaging, an appropriate plan of care can be rapidly implemented to diagnose, define, and possibly treat a patient presenting with an acute stroke (Fig. 2.4).

In recent years, the medical community has made a concerted effort to reduce the incidence of stroke by identifying patients most at risk. Much effort has been expended to identify risk factors for atherosclerotic disease, and new strategies have been developed to reduce the rate of stroke in high-risk patients [46]. Efforts range from modification of lifestyle to preemptive surgical or endovascular carotid artery intervention. Randomized, prospective clinical trials that include imaging and other criteria have shown that surgical endarterectomy is effective in reducing stroke morbidity of both asymptomatic and symptomatic patients [47–52].

Imaging today offers a number of sensitive, noninvasive and therefore low risk, tests, all directed at diagnosing the most common cause of a stroke—carotid artery atherosclerosis—in “at risk” patient groups such as those with a carotid bruit [53, 54]. While duplex ultrasound (US) and computed tomography angiography (CTA), magnetic resonance angiography (MRA) and time-resolved contrast enhanced MRA (CE-MRA) all have high diagnostic accuracies for detecting internal carotid stenosis, 70–99 % [55, 56], only US appears to offer cost-effective initial screening. However, given the operator imaging variability with sonography as well as the artifact created from calcified plaques, and the difficulty in distinguishing subtotal from total occlusion, a full endorsement of its routine use as the sole examination before endarterectomy cannot be made [55, 57]. Most radiologists today recommend combined use of US with CE-MRA [53–55, 57–59].

Multi-slice CTA offers an alternative means of examination; however, it poses risks from intravenous iodinated contrast administration. CTA requires a large intravenous contrast injection volume and hence has the potential for contrast-induced nephrotoxicity or anaphylaxis. In addition, CT exposes the patient to an ionizing radiation dose. CTA also may be less accurate at evaluating the degree of luminal narrowing in the presence of calcified plaque than some other techniques [56, 60, 61].

It is hoped that better plaque characterization will improve the predictive value of imaging at identifying clinically significant carotid stenosis for patients with symptomatic cerebral ischemia [62, 63]. A variety of imaging strategies could be undertaken in symptomatic patients at risk for major ischemic stroke, where the initial study could include a brain imaging examination, quickly followed by one of the abovementioned noninvasive vascular studies.

In patients with chronic carotid stenosis or occlusion, the elevated ischemic stroke risk could be further evaluated by functional imaging. With perfusion imaging, CBV and CBF can be quantitatively and qualitatively assessed. In the recent past, this was performed with a nuclear SPECT flow study during a rest and “challenge” phase following the administration of Acetazolamide. This same principle also can be utilized with ¹⁵O-PET where the oxygen extraction differences pre- and post-challenge permit calculation of cerebral vascular reserve (CVR) [64–66]. It has been shown that CVR inversely correlates with stroke risk. Low CBV measurement by either CT or MR appears to correlate with reduced CVR and increased stroke risk [67, 68]. Compared with other examinations, CT and MR are becoming more widely accepted for functional assessment of the at-risk brain tissue because they are more widely available than PET, have better resolution than SPECT, and have overall shorter study times compared to nuclear imaging in general.

Since the advent of reperfusion therapies, acute ischemic stroke has been transformed from incurable and nonurgent to most emergent and critically treatable. As discussed above, the ability to treat acutely ischemic tissue has impelled physicians to develop a method by which they could distinguish viable from nonviable brain parenchyma.

Current clinical practice in the United States is based on the 1996 FDA approval of intravenous (IV) rtPA therapy. Once cerebral hemorrhage has been excluded using NCCT, the drug is administered, preferably within 1 h and no later than 3 h after symptom onset. As a part of accepted protocol, acute stroke must obtain the NCCT within 25 min of admission and expert interpretation within the next 20 min (45 min “door-to-interpretation” time) [69]. Recent increases in public awareness, faster emergency medical response, and establishment of dedicated stroke centers have resulted in 19–60 % of admissions arriving at treatment centers within 3 h of symptom onset.

Despite these efforts, only 3–8.5 % of ischemic stroke admissions qualify for rtPA therapy [70–72]. Because of the small numbers of acute stroke patients qualifying for treatment within the current 3-h limit, interest in expanding the treatment window has been growing if it can be shown not to increase the risk of hemorrhage. A pooled risk-benefit analysis of existing rtPA trials using NCCT scan for the exclusion of hemorrhage has suggested that rtPA may be safe in some patients out to 4.5 h after stroke, but the FDA and ASA recommendations have not yet been modified to include this expanded treatment window in published guidelines. The American College of Radiology (ACR) appropriateness criteria may change in the very near future as the results of these studies and trials become conclusive.

There is growing evidence that intra-arterial (IA) thrombolytic delivery and mechanical clot extraction methods are beneficial either alone or with IV rtPA therapy in patients who fall outside the 3-h limit or who have large-vessel occlusion or larger clot burden. They may be at a higher risk of hemorrhage, however. Furthermore, complexities of organizing these later stage therapies have limited their widespread adoption in general [73–75, 76].

Many centers now routinely perform CT perfusion, but currently there is no clear consensus on whether the information obtained from CTP should be used to guide intravenous (IV) or intra-arterial (IA) therapy. MR perfusion and diffusion imaging could be performed instead, but unfortunately this technique is time-prohibitive and not universally available on a 24 h/7days a week basis. Furthermore, contraindications listed previously (Table 1.​3, Chap.​ 1) may preclude patients from having an MR.

It should be noted that in addition to NCCT to exclude acute hemorrhage in new onset stroke patients, previously described multimodality MRI and CT studies also may be useful to confirm the diagnosis, classify the subtype of stroke, demonstrate lesion location, identify vascular occlusion, and guide other management decisions both within and beyond the 3 h period. Currently, however, ASA and others’ guidelines specifically recommend that emergency IV rtPA treatment within the 3 h window not be delayed in order to obtain multimodality imaging studies and furthermore that treatment not be withheld on the basis of either negative or additional positive MR or CT findings, other than acute hemorrhage [77–81].

While the discovery of an intracranial mass lesion may be incidental, patients can present with focal or non-focal neurologic deficits. Signs or symptoms may range from headaches, seizures, syncope, to change in mental status. Clinical history along with imaging can provide a framework for proper categorization of the disease process. General categories for possible etiologies of an intracranial mass lesion include infectious, inflammatory, traumatic, vascular, or neoplastic. Contrast utilization is often quite helpful not only in characterizing the disease process but also evaluating the full anatomical extent of disease. While the role of imaging initially was limited to providing anatomic details, the present role is to provide functional information through a vast array of modalities such as perfusion, diffusion, MR spectroscopy, and PET [82]. Sophisticated imaging techniques allow insight into such processes as the free movement of water molecules, microvascular integrity, chemical composition, and glucose metabolism of the lesion. Merging the morphologic and functional information gained from these advanced imaging techniques can then provide a more comprehensive assessment of the lesion so that we may better understand its physiology and in turn predict its behavior (Fig. 2.5).

Since CT is highly accurate for the diagnosis of acute hemorrhage, it has been the mainstay in emergent evaluation of acute intracranial bleeding, especially subarachnoid or parenchymal hemorrhage, both of which are associated with high morbidity and mortality [83, 84]. In the case of SAH caused by aneurysms, the high morbidity rate is partly due to a high likelihood of re-bleeding. Early surgical intervention or intravascular coiling is recommended to reduce morbidity. Before therapy can be undertaken, a cerebral angiogram is required to define the aneurysm’s location and morphology. Studies show that catheter-based angiography has approximately 90 % sensitivity in detecting an aneurysm. This sensitivity, however, decreases to approximately 80 % in the setting of SAH resulting from small aneurysm size or in the face of aneurysm thrombosis, local vasospasm, or an incomplete study [85, 86]. Traditionally, non-visualization of an aneurysm on the initial scan from any of the above reasons warranted a follow-up catheter-based repeat angiogram 1 week after the initial examination. The clinician should be aware that the cost and risk to obtain the additional 1–2 % diagnostic yield has been debated [87].

Today, clinical practice has shifted toward initial NCCT for SAH detection and if found immediate CTA for aneurysm detection. Studies have shown that CTA has overall detection sensitivities of 85–95 % for aneurysms greater than 2 mm in diameter [88–90]. Today, treatment of intracranial aneurysms following SAH is increasingly based on CTA alone [91, 92]. In addition, the appearance of new neurologic changes suggestive of post-SAH vasospasm, ischemia, or hydrocephalus is increasingly investigated with transcranial Doppler (TCD) and CT imaging with CTA and CTP. Catheter angiography and 123I-IMP SPECT are used less frequently than in the past [85, 93–98].

In the absence of predisposing risk factors such as family history, polycystic kidney disease, connective tissue disorder, or collagen vascular disease, the need to screen the general population for aneurysms is debated. Proponents raise concerns over the cumulative long-term risk of morbidity and mortality from SAH, particularly for aneurysms larger than 2.5 cm. When this is weighed against the relatively low risk of clipping and coiling unruptured intracranial aneurysms, data suggest that there may be a clinical role for prophylactic aneurysm screening [99, 100

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