To the present day, the first and most widespread diagnostic approach in the assessment of acute stroke remains computed tomography (CT) scans. Its sensitivity is very high (nearly 100%) in detecting intracerebral hemorrhage in the acute period, but its capability of revealing ischemic injury in the very first hours after symptom onset is relatively poor. On the other hand, perfusion CT and newer magnetic resonance (MR) imaging techniques such as diffusion-weighted and perfusion-weighted imaging (DWI and PWI respectively) permit a more detailed evaluation of the pathophysiology of stroke and therefore can lead to better management. These improvements are due to the better sensitivity of these diagnostic tests in the acute phase of stroke that can detect ischemic lesions and their ability to estimate tissue perfusion to determine the vascular status. Since patients with ischemic penumbra, i.e. tissue with impaired function but preserved morphology, are more likely than those without to respond to thrombolytic therapy, identification of patients with this feature will become increasingly important. In this review, we present briefly the current role and limitation of CT and conventional MRI. We also address the possible applications of perfusion CT and other MR techniques, such as MR angiography, MR spectroscopy, DWI and PWI in the diagnosis of acute stroke. 

Keywords: stroke; computed tomography, magnetic resonance, cerebral infarction;  penumbra, thrombolysis

Introduction:

Cerebral ischemic stroke is one of the most fatal diseases despite current advances in medical science. Patients presenting with suspected stroke require rapid diagnosis and treatment. Conventional CT and MR imaging are not sufficiently sensitive to evaluate stroke in the hyper acute stage. CT may be adequate to detect intracranial hemorrhage, but in the case of nonhemorrhagic stroke, the CT scan may be negative for the first 24 to 36 hours [1]. Conventional MR scans can detect acute stroke by 6 to 12 hours. But new stroke therapies such as intra-arterial and intra-venous thrombolysis with recombinant tissue plasminogen activator (rt-PA) focus on the first 3 to 6 hours after stroke symptom onset. However, DWI, PWI and MR spectroscopy can detect cerebral ischemia as early as 45 minutes after middle cerebral artery occlusion [2]. Most pharmacological interventions in the acute phase of ischemic stroke are based on the concept of ischemic penumbra, a region of reversible ischemia that is still viable but will eventually evolve to infarction [3]. The ultimate goal for imaging is to define the area of brain infarction and perfusion deficit, and to identify any ischemic tissue that can be salvaged by medical or surgical therapy. This review starts with the various imaging modalities of ischemic stroke and goes on to explore the recent advances in this field. The findings of ischemia and infarction on other imaging modalities such as angiography, single photon emission computed tomography (SPECT), positron emission tomography (PET), xenon CT and magnetoencephalography are not reviewed here.

Computed Tomographic Imaging of acute stroke

Conventional CT findings

Computed tomography (CT) has revolutionized the assessment of patients who present with an acute neurological deficit with the head CT scan now playing an integral role in the screening and treatment of stroke patients (Fig.1A). It is fast, reliable, readily available, and continues to be used for all major stroke therapy trials.
CT images are obtained by projection of a high-kilovolt age collimated beam through the brain. Beam attenuation is due to absorption proportional to the linear attenuation coefficient of the materials through which it passes. The relatively high-kilo voltage x-rays used in CT result in linear attenuation primarily due to tissue density. Differentiation of adjacent tissues such as gray matter and white matter depends on perceivable differences in electron density; detection of a pathologic condition requires a perceivable change in electron density. The non-contrast head CT scan remains the first-line imaging study in suspected stroke patients due to its ubiquity and exquisite sensitivity for the detection of blood. CT has demonstrated to have nearly 100% sensitivity for the detection of intraparenchymal hemorrhage [1]. 

There are four possible signs on CT when a patient presents with an acute neurological deficit in order to make a diagnosis of ischemic stroke: 

A. Hyperdense Artery Sign: When an artery (typically MCA, PCA, or ACA) appears hyperdense, this is indicative of a major occlusion of the vessel with thrombus formation 
B. Loss of Insular Ribbon ("Insular ribbon sign"): The insular ribbon is an area of extreme gray-white differentiation that is readily examined on the CT scan. Loss of the insular stripe is one of the more subtle early indications of MCA stroke. 
C. Loss of cortical gray-white differentiation
D. Mass effect: Swelling visible within the first 6 hours indicates severe edema and indicates a poor prognosis for the majority of patients.
The use of intravenous contrast infusion for CT evaluation of acute ischemic stroke is controversial. There is no evidence that use of contrast increases the yield of CT in patients with acute ischemic stroke, and there is a theoretical concern about promoting cerebral "toxicity" in the face of an acutely disturbed blood-brain barrier in large infarcts [4].

Although CT may show findings of infarction as early as 3-6 hours after ictus, up to 60% of CT scans are normal in the first few hours after ischemic insult. Thus, despite some reports of high sensitivity in the acute period, it is still accepted that its overall sensitivity is relatively poor [5]. Although new imaging techniques such as DWI, PWI and xenon CT have shown considerable promise in the detection of early brain ischemia, noncontrast CT remains the primary imaging test for the evaluation of acute stroke. Despite its limitations, CT is an accurate method of screening patients prior to thrombolytic therapy [6].

Perfusion CT

Perfusion CT has recently been introduced in the clinical routine for the diagnostic workup of stroke patients. Based on the indicator dilution principle, the perfusion CT option allows the quantitative evaluation of dynamic CT data of the brain following the injection of a compact bolus of iodinated contrast material. By providing images of cerebral blood flow (CBF), cerebral blood volume (CBV) and mean transit time (MTT) from one set of dynamic CT images, perfusion CT allows a quick and reliable assessment of the type and extent of cerebral perfusion [7] (Fig.1B and 1C). A "CBF/CBV mismatch", in perfusion CT is analogous to "perfusion/diffusion mismatch" in MR imaging, and is a good indicator for the ischemic margin surrounding the core of infarction. Thus, in addition to confirming perfusion disturbances of the brain, perfusion CT is used increasingly to distinguish the core of infarction and peri-infarct ischemia (so called penumbra) [8]. 

MR Imaging of acute stroke

MR imaging techniques are being increasingly used in the evaluation of stroke. But, the, ability of conventional MR sequences to identify the location and extent of infarction. is rather poor. The advent of new MRI techniques such as DWI and PWI has revolutionised diagnostic imaging in stroke during the critical initial hours after the onset of ischemic stroke. MR offers three essential features in the diagnosis of stroke: 1) vascular lesion identification, 2) delineation of injured brain tissue, and 3) map of ischemic brain. 
MR imaging involves placing a patient in an applied external magnetic field. Because of the precessional properties of those nuclei with an odd molecular mass or odd charge, the most abundant of which is hydrogen, the nuclei will act as small magnets that align with the magnetic field. With the use of applied radio-frequency pulses and receiver coils, it is possible to generate and detect different signals from tissue based on the number of protons per unit volume (spin density) of different substances. MR techniques can noninvasively measure specific parameters that are sensitive to the biophysical environment of water in the tissue. These include the water 1H spin-lattice (T1) and spin-spin (T2) relaxation times; spin density, and apparent (translational) diffusion coefficient of water (ADC). MR imaging readily identifies change in the 1H related MR parameters of water that occur following ischemic stroke. 

Conventional T1- and T2-weighted sequences

With standard T1-weighted sequences, the earliest finding of ischemia within minutes of onset is loss of normal vascular flow void phenomena, which can sometimes be detected in large arteries [9]. Post contrast T1-weighted sequences using gadopentetate dimeglumine has better sensitivity in the detection of early cerebral ischemia [10]. Arterial enhancement is the earliest finding and sometimes can be detected within minutes after onset of ischemic symptoms (Fig. 2A). Slow antegrade or retrograde (collateral) flow is thought to be the likely mechanism for arterial enhancement seen with early cerebral ischemia. 
Conventional T2-weighted sequences are not reliably sensitive in detecting ischemia in the first few hours after symptom onset (Fig.2B). The development of signal change on T2-weighted images is caused by the early increase in overall brain water content with acute ischemia.

Fluid-attenuated inversion recovery sequence (FLAIR)

The FLAIR MR imaging sequence produces a heavily T2-weighted image with nulling of the signal of cerebrospinal fluid using an inversion time usually of 1800 to 2500 msec. By suppressing the signal intensity of bulk water, FLAIR MR images increase the conspicuity of lesions located in areas adjacent to or filled with cerebrospinal fluid. This property gives FLAIR its distinctive characteristics. There are few unique signs observed in FLAIR images during the first 24 hours after the onset of stroke symptoms [11].
Increased signal in the lumen of large and small vessels may be observed on FLAIR images as the only indication of infarction, a finding that has been called the 'hyperintense vessel sign' or arterial hyperintensity [12](Fig. 2C). The sensitivity of hyperintense vessel sign is maximum in the first 6 hours after the symptom onset thereafter the detection rate is declining over time [13].
Acute cerebral infarcts can appear in the FLAIR image as swollen cortical gyri of increased signal intensity [12]. Typically these gyriform areas are moderately hyperintense and are not sharply demarcated. Slightly prolonged T2 relaxation of edematous cortical gyri is shown as areas of high signal intensities both on FLAIR and T2-weighted images. FLAIR demonstrates these areas more clearly than T2-weighted images by suppressing the signal of the cerebrospinal fluid in the adjacent cortical sulci and the neighboring brain parenchyma.

MR Angiography 

MR angiography (MRA), a major advance in ischemic imaging technique is very sensitive to flow and is based on the difference in signal between moving blood and stationary brain tissue. The three-dimensional (3D) time-of-flight (TOF) technique is based on flow-related enhancement and is the preferred MRA technique. However, it has some limitations, especially flow signal dropout secondary to turbulent flow in the tortuous and stenotic vascular segments, which makes interpretation of stenos is in these areas difficult. Also, in slow-flow regions, the spin saturation of the scan causes overestimation of stenos is. Two-dimensional (2D) TOF MRA also depends on the relative contrast between flowing blood and stationary tissue; it provides better images than 3D TOF in slow-flow regions. 2D TOF images correlate well with carotid angiography images in depicting cervical bifurcation disease. Its disadvantages, however, are the significant artifacts (e.g., stepladder) that often occur, which may obscure vessel details, and the longer scanning time. The modified TOF MRA technique, which uses multiple, overlapping thin slab acquisitions (MOSTA), combines the advantages of 2D and 3D TOF techniques. Two-dimensional phase-contrast (PC) MRA is a technique that is helpful specifically in differentiating slow and absent flow from normal flow and it captures only truly patent vessels. Since MRA techniques have a high negative predictive value, a normal or near-normal MRA of the carotid arteries can effectively exclude the possibility of high-grade carotid stenos is [14]. The anatomy of the circle of Willis, as well as its fast arterial flow, lends itself well to both 3D TOF and 2D or 3D phase-contrast (PC) MRA in the evaluation of cerebrovascular ischemic disease (Fig.2D). Compared with precontrast 3D TOF MR angiograms, postcontrast 3D TOF angiograms improve assessment of intracranial vessel patency in acutely ischemic vascular territories [15]. The use of paramagnetic extracellular contrast agents, such as gadopentetate dimeglumine, shortens the T1 relaxation time of blood and thereby increases the steady-state signal intensity of the blood above that of most stationary tissues.

MR Spectroscopy

MR spectroscopy (MRS) is a non-invasive in vivo method that allows the investigation of biochemical changes in both animals and humans [16]. Any nucleus with a nonzero nuclear spin has the ability to generate an MR signal; thus metabolic derangements induced by ischemia can be depicted with MRS [17]. MRS studies of cerebral ischemia have been confined primarily to proton (1H) and phosphorus (31P) nuclei because of their natural abundance. 1H MRS can depict an increase in lactate concentration and concomitant decrease in intracellular pH in the hyperacute ischemic stage. It was shown on MRS that N-Acetylaspartate (NAA) located solely in neuronal bodies has been depleted from infarcted tissue [18]. Thus areas of the brain that have elevated lactate concentrations with normal levels of NAA may represent ischemic tissue that is potentially salvageable. 31P MRS can detect subtle frequency differences between various phosphate nuclei. Immediately after an acute ischemic insult, there is progressive loss of high-energy intracellular ATP and phosphocreatine (PCr), with resultant decreases in the phosphocreatine/ inorganic phosphate (PCr/Pi) ratio. 31P MRS can detect these alterations within minutes after the onset of ischemia. However, the clinical utility of MR spectroscopy is hampered by long acquisition time, motion artifacts and time-consuming post-processing.

Diffusion-weighted imaging 

Diffusion -weighted imaging (DWI), first described by Le Bihan is sensitive to the microscopic motion of water protons [19]. Protons in moving water molecules undergo a phase shift of their transverse magnetization in the presence of a magnetic field gradient. A diffusion-weighted image can be obtained by incorporating strong diffusion sensitizing gradients into a conventional spin-echo sequence. The resulting image reflects signal alteration caused by water proton diffusion and T1 and T2 relaxation effects. Thus areas of greater diffusion (fast) are subject to a greater degree of signal attenuation compared with areas of diminished diffusion (slow), which have less signal attenuation. Increasing the duration and amplitude of the gradients increases the sensitivity of MRI to the molecular diffusion of water. The apparent water diffusion coefficients (ADC) can be calculated from acquisitions with different diffusion weightings. A measure for the diffusion weighting is the b-value. The b-value increases with the strength, duration and temporal separation of the two diffusion-sensitive gradient pulses.
In acute stroke, there is reduction in the diffusibility of water, apparently related to the movement of extracellular water into the cell due to membrane pump failure. The intracellular environment contains organelles and macromolecules that restrict movement of water. This results in a logarithmic increase in signal intensity, so that areas of acute infarction are hyperintense (Fig.3A) on DWI images. Calculated ADC maps demonstrate a 40%-50% reduction in water movement in corresponding areas of acute infarction [20] (Fig.3B). DWI and ADC changes are observed within the 1st hour after ictus and remain positive during the initial 6-12 hours. Maximum signal intensity at DWI is demonstrated at about 24-48 hours. DWI signal intensity remains increased during the first 7-14 days, with a gradual decline over a time course of weeks to months, corresponding to rising ADC values. DWI is highly accurate for diagnosing stroke within 6 hours of symptom onset and is superior to CT and conventional MR imaging [21]. There is high correlation between the volume of early DWI lesions with clinical neurological outcome as well as final infarct volume as measured by T2-weighted imaging. Thus, DWI may facilitate optimal selection of patients for new medical therapies of stroke and may provide a highly sensitive technique for evaluating the efficacy of new treatments [22].

Perfusion-weighted imaging 

The dynamic susceptibility contrast-enhanced perfusion weighted imaging (PWI) for evaluation of tissue perfusion was first proposed by Villringer [23, 24]. When placed in a magnetic field, the gadolinium contrast agent decreases T1 and T2 in tissues in which it accumulates. T1 shortening, which has been called the R1 effect, results in increased signal intensity on T1-weighted images. R2 effects produce shortening of T2 or T2* relaxivity, which represents loss of phase coherence of transverse magnetization, resulting in intravoxel signal loss due to magnetic susceptibility. Bolus contrast perfusion MR imaging is based on R2 effects resulting from the production of magnetic field gradients between the lumen of a vessel and surrounding tissue. The susceptibility effect extends an additional capillary radius beyond the carrying blood vessel and is well suited for the evaluation of cerebral perfusion. Contained within the lumen by an intact blood-brain barrier, the bolus of gadolinium is considered a nondiffusible tracer during the first pass though the cerebral circulation. 

After bolus injection of lanthanide contrast agent, sequential images are obtained at 1-2-second intervals during the first pass through the cerebral circulation. MR perfusion studies use paramagnetic or superparamagnetic susceptibility contrast agents, such as gadolinium or dysprosium chelates, or iron oxide particulates. These agents induce signal alteration in regions of the brain where they are delivered. The intravascular compartmentalization of these agents results in magnetic susceptibility-induced T2* shortening. On perfusion images the T2-susceptibility effect is long-range, extending well beyond the vessel lumen and into the adjacent brain tissues. Thus perfusion MRI depicts the passage of contrast through the cerebral microcirculation. F
Calculations and mapping are performed on a per pixel basis by using the susceptibility change-versus-time curves. Thus, dynamic, ultrafast perfusion MRI can offer semiquantitative analysis of cerebral perfusion. By using contrast concentration-time curves, the regional cerebral blood volume (rCBV) and regional cerebral blood flow (rCBF) can be calculated (Fig.3E-H). 

Cerebral blood volume (CBV) describes the volume of the cerebral capillaries and venules. CBV is directly obtained from tracer MR measurements by mathematical integration of the area under the susceptibility curve during the first pass of the lanthanide contrast agent. Decrease in signal intensity is proportional to blood lanthanide concentration in brain capillaries and venules. 
Cerebral Blood Flow (CBF) represents instantaneous capillary flow in tissue and may be calculated from the curves obtained in small animals but is mathematically challenging in humans. Owing to larger bolus dispersion, the determination of physiologically valid CBF in humans may require the addition of arterial input flow data. Currently, these techniques are not widely available.

Mean transit time (MTT) is the measure of the length of time a particle spends in the cerebral capillary circulation. These parameters are related by the central volume equation 
MTT = CBV/CBF

The change in signal over time is used to calculate displays of CBV (Fig.3E), CBF (Fig.3F) and MTT (Fig.3G). It should be understood that perfusion imaging is technically challenging and have inherently lower resolution than other MR techniques. Furthermore, absolute perfusion cannot be reliably measured with current MR techniques. This is because the arterial input function is neither known nor estimated with the standard MR perfusion techniques. So, only relative regional perfusion characteristics such as rCBV, rCBF, and rMTT, are derived from dynamic MR imaging data, which can be used for further analysis.

For stroke, multisection imaging with full brain coverage is achieved with rapid, single-shot imaging sequences such as echo-planar imaging. MR perfusion imaging can be used to detect early ischemic changes with much higher sensitivity than that of conventional MR imaging. The mean transit time map shows decreased perfusion and the size of the total ischemic region (both the infarct core and the surrounding ischemic area)25. Brain territories with decreased cerebral blood volume are associated with irreversible infarct. Increased cerebral blood volume may indicate the presence of collateral flow or infarct reperfusion. It has also been reported that the area of perfusion abnormality often exceeds the area of diffusion abnormality, and that this mismatch may represent the ischemic penumbra [26]. Typically, the ischemic penumbra is partially recruited into the ischemic core during the first hours after symptom onset. Since PWI is very sensitive in detecting perfusion deficits, the PWI/DWI mismatch region (penumbra) may comprise not only tissue at risk but also hypoperfused tissue with CBF values above the critical viability thresholds [27].

There is lot of research ongoing that relates the perfusion parameters with the fate of the ischemic tissue in order to determine the viability thresholds of hypoperfusion [28,29]. Identifying tissue at risk for infarction is important in deciding which patients would benefit most from potentially harmful therapies and provides a way to evaluate newer therapies with regard to the amount of ischemic tissue salvaged [30].

Conclusions

With the advent of multidetector CT advanced stroke protocols combining plain CT, and perfusion CT can routinely be accomplished within a very short time span thus ensuring the role of CT in the diagnostic workup of acute stroke. A comprehensive evaluation of cerebral ischemia is possible with advanced MR techniques. Diffusion techniques provide early delineation of the extent of tissue that is likely to proceed to infarction. Perfusion and spectroscopy aid in delineating the area at risk of infarction, and MR angiography can help determine if there is a thrombus amenable to lysis. 

Figures

A	B	C
Figure 1: 76-year-old female patient with complete aphasia and right-sided hemiplegia was admitted 35 minutes after onset of symptoms. A. Nonenhanced CT does not demonstrate "early signs" of acute ischemic stroke. B, C. CT perfusion demonstrates large region of reduced perfusion, indicating potentially viable brain tissue with functional impairment.
A	B	C
	A, Post-contrast T1-weighted image shows vascular enhancement in insular branches of left middle cerebral artery. B, However, T2-WI at this point does not show any abnormality. C, FLAIR shows tubular area of hyperintense signal in M2 segment of left middle cerebral artery corresponding to slow flow or thrombosis D Three-dimensional time-of-flight MR angiography confirms absence of normal flow in left middle cerebral artery
D
Figure.2: Hyperintense vessel sign and intravascular contrast enhancement in 68-year-old woman with right-sided weakness. MR imaging was performed within 4 hours of symptom onset.
A	B	C
D	E	F
G	H
Figure.3: 52 year old man presenting with sudden onset right right sided weakness.MRI was performed within three hours of symptom onset.A: T2-WI is normal during this early stage. B: MRA shows lack of flow in the M2 srgment of left MCA. C: DWI reveals acute infarct as are of hyperintensity in the left posterior temporal lobe. C: Corresponding ADC map shows early ischemia as region of hypointensity.In the PWI- regional cerebral blood volume(rCBW), regional Cerebral Blood Flow (rCBF) and mean transit time (MTT) maps [figures E,F,G respectively] perfusion parameters are determined in the core (L1), penumbra (L2) and normal contralateral side (L3). H: Time intensity curve corresponding to 3 regions of interest (ROIs) [L1(red)=core; L2(pink)=penumbra; L3(blue)=normal contralateral side]

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