Intracranial Hemorrhage Evaluation with MRI 

Intracranial Hemorrhage Evaluation with MRI 

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The appearance and evaluation of intracranial hemorrhage on MRI (see the images below) primarily depend on the age of the hematoma and on the imaging sequence or parameters (eg, T1 weighting, T2 weighting). [1] Other influences are the site of the hemorrhage, the local partial pressure of oxygen in the tissues, the local pH, the patient’s hematocrit, the local glucose concentration, the hemoglobin concentration, the integrity of the blood-brain barrier, and the patient’s temperature. [2, 3, 4, 5]

Intracranial hemorrhage (ICH) is a common cause of acute neurologic emergency. Pathologic accumulation of blood in the cranial vault (ie, ICH) may occur in the brain parenchyma or the surrounding meningeal spaces. Such accumulations can be epidural hematomas (EDHs), subdural hematomas (SDHs), subarachnoid hemorrhages (SAHs), or intraventricular hemorrhages (IVHs).

The etiology of ICH is multifactorial and varies with a person’s age and predisposing factors.

CT has traditionally been used in the radiologic workup of ICH (see the image below). However, numerous studies have demonstrated that MRI is more efficient in detecting ICH and in localizing ICH. In addition, MRI can provide important clues about the etiology. [6]

According to one study, MRI identifies small volumes of IVH in cases not detected by CT and yields higher estimates of intraventricular blood volume. The study data indicated that consideration of technical differences is needed when comparing images from the 2 modalities in the evaluation for IVH. CT failed to detect IVH in 3% of cases, whereas MRI was 100% sensitive. MRI and CT yielded equal Graeb scores in 72% of the pairs, and MRI Graeb score was higher in 24%. [7]

Intracranial vessel wall MRI allows visualization of the artierial wall. [8, 9, 10, 11] The Vessel Wall Imaging Study Group of the American Society of Neuroradiology has provided consensus recommendations for current clinical practice of intracranial vessel wall MR imaging as an adjunct to conventional angiographic imaging with CTA, MRA, or DSA. According to the study group, vessel wall MRI has multiple potential uses in the context of ischemic stroke and intracranial hemorrhage, such as the following [9] :

To differentiate between intracranial atherosclerotic plaque, vasculitis, reversible cerebral vasoconstriction syndrome, arterial dissection, and other causes of intracranial arterial narrowing.

To determine the location of atherosclerotic plaque relative to branch artery ostia, to diagnose stroke etiology, and to assess risk of angioplasty.

To predict future behavior of unruptured intracranial saccular aneurysms.

To identify symptomatic, nonstenotic disease of the intracranial arteries.

To assess atherosclerotic plaque activity.

To assess vasculitis activity.

To select an intracranial target for biopsy in suspected CNS vasculitis.

To determine which aneurysm has ruptured in patients with acute subarachnoid hemorrhage and multiple aneurysms.

As a hematoma ages, hemoglobin changes through several forms oxyhemoglobin, deoxyhemoglobin, and methemoglobin before the RBCs are broken down into ferritin and hemosiderin. [1]

Five distinct stages of hemorrhage can be defined (see Table 1, below).

Table 1. Stages of Hemorrhage (Open Table in a new window)

Phase

Time

Hemoglobin, Location

Hyperacute

< 24 h

Oxyhemoglobin, intracellular

Acute

1-3 d

Deoxyhemoglobin, intracellular

Early subacute

>3 d

Methemoglobin, intracellular

Late subacute

>7 d

Methemoglobin, extracellular

Chronic

>14 d

Ferritin and hemosiderin, extracellular

 

Goals of MRI in the evaluation of intracranial hemorrhage (ICH) are as follows:

To recognize the presence of blood

To localize and differentiate hemorrhages (extra-axial versus intra-axial): if extra-axial, to differentiate subarachnoid hemorrhage (SAH), subdural hematoma (SDH), and epidural hematoma (EDH); if intra-axial, to locate the specific neuroanatomic site

To determine the age of the hemorrhage

To identify the etiology

To aid in managing the bleed and in ascertaining the patient’s prognosis

Diamagnetic materials are substances that do not have unpaired electrons in the atomic and molecular orbitals. These materials reduce the magnitude of an applied magnetic field. More than 90% of human tissues—including oxyhemoglobin—are diamagnetic. [2]

Paramagnetic substances are substances with unpaired electrons in their atomic or molecular orbitals. These materials have no intrinsic magnetic field in the absence of an applied magnetic field, but they can augment an applied field when they are exposed to it. Examples of paramagnetic substances are copper, iron, manganese, and gadolinium. [2]

On MRI, the signal intensity of a hemorrhage depends on both the chemical state of iron (ferrous or ferric) in the hemoglobin molecule and on the integrity of the RBC membrane. [12]

Iron can be either diamagnetic or paramagnetic, depending on the state of its outer-orbital electrons. In the paramagnetic state, iron alters the T1 and T2 relaxation times of water protons as a result of magnetic dipole-dipole interaction and susceptibility effects. This dipole-dipole interaction shortens both T1 and T2 relaxation times, with a greater effect on T1 than on T2.

A susceptibility effect is present when iron atoms are compartmentalized in the RBC membrane. There, they cause inhomogeneity of the magnetic field, with a resulting loss of phase coherence and with selective shortening of the T2 relaxation time. After the RBC membrane degrades, the iron becomes more homogeneously distributed than before, and this effect is nullified. [2]

The variable appearance of hemorrhage on MRI depends on the structure of hemoglobin, on its various oxidation products, and on whether unpaired (ie, paramagnetic) electrons are present. [2]

Table 2 (see below) summarizes electronic and magnetic properties of relevant substances of MRI in ICH.

Table 2. Electronic and Magnetic Properties of Substances Relevant to MRI of ICH (Open Table in a new window)

Substance

No. of Unpaired Electrons, e

Magnetism

Oxyhemoglobin

0

Diamagnetic

Deoxyhemoglobin

4

Paramagnetic

Methemoglobin

5

Paramagnetic

Hemosiderin

5

Paramagnetic

Ferritin

5

Paramagnetic

Gadolinium

7

Paramagnetic

 

States of intraparenchymal hematoma include the following:

Hyperacute hemorrhage (see the following image)

Acute hemorrhage (see the following image)

Early subacute hemorrhage (see the following image)

Late subacute hemorrhage (see the following image)

Chronic hemorrhage (see the following image)

Freshly extravasated erythrocytes from the arterial blood contain fully oxygenated hemoglobin with unpaired electrons. Hence, oxygenated blood is diamagnetic. In the absence of a paramagnetic component, no proton-electron dipole-dipole interaction occurs, and no paramagnetic relaxation enhancement is observed. Therefore, the bulk of the hyperacute hematoma appears identical to most brain lesions on MRI. [2]

Hyperacute hemorrhage appears slightly hypointense or isointense relative to the brain on T1-weighted images and slightly hyperintense to the brain on T2-weighted images. T2-weighted MRI images may show a thin, irregular rim of marked hypointensity; this is attributed to rapid deoxygenation at the blood-brain interface. This hypointensity is marked on T2-weighted gradient-echo images. Such lesions do not enhance after the administration of a gadolinium-based contrast agent. On diffusion MRI, the lesion demonstrates restricted diffusion compared with normal brain parenchyma. [13, 14]

The acute phase begins after a few hours and is characterized by the formation of deoxyhemoglobin. This process first occurs in the periphery and then affects the center. The iron atom in deoxyhemoglobin has 5 unpaired electrons; hence, it is paramagnetic. The magnetic susceptibility of deoxyhemoglobin is different for intracellular and extracellular locations. Acute hematoma contains intracellular deoxyhemoglobin and appears markedly hypointense on T2-weighted MRI images. At high-field strengths, T2-weighted images—and especially gradient-echo images—depict marked hypointensity.

During the acute phase, the clot retracts, increasing the hematocrit and surrounding edema, which appears as a hyperintense perilesional rim on T2-weighted MRI. The increased hematocrit causes a parallel increase in T1 and T2 relaxation times.

With an acute hematoma, T1-weighted images show isointensity or slight hypointensity. This appearance is observed because the 3-dimensional structure of deoxyhemoglobin blocks the access of water protons to iron atoms and thus prevents the magnetic dipole-dipole interaction. Hence, the T1 relaxation time is not shortened. A thin hyperintense rim is sometimes seen in the periphery; this is caused by early oxidation of deoxyhemoglobin to methemoglobin. [2, 15]

In a study of acute intracranial hemorrhage in pediatric patients with head trauma, rapid MRI was found to have only modest results in detection of subdural and epidural hemorrhages without prior CT (sensitivity 61-74%), but results improved if a prior CT  had been done (sensitivity 80-86%). As a result, according to the study, rapid MRI is not adequate to replace CT in initial evaluation of intracranial hemorrhages in pediatric patients but may be helpful in follow-up of known hemorrhages. [16]

In a study of patients with acute intracerebral hemorrhage, multiparametric MRI was able to identify neuroinflammation to facilitate early-phase development of anti-inflammatory treatments, as inflammation can be a major contributor to secondary injury after intracerebral hemorrhage. [17]

The early subacute phase begins after 2-7 days. An inflammatory cell response can be observed in the surrounding tissues. Macrophages invade the boundary of the hematoma to clear extravasated material and damaged tissue. When low oxygen tension continues, the amount of reducing substances declines. This change causes a failure in RBC metabolism, and iron atoms are oxidized to the ferric state. The result is the formation of methemoglobin and, thus, exposure of the iron atoms to water protons. This pattern decreases the T1 relaxation time and leads to marked hyperintensity on T1-weighted MRI.

A susceptibility effect is present because the RBC membrane remains intact. Hence, continued hypointensity is observed on T2-weighted images. [15]

Over several days to weeks, the energy status of the RBC declines, causing a loss of cellular integrity, and the cells lyse. This event marks the beginning of the late subacute phase. As the loss of RBC integrity removes the paramagnetic aggregation responsible for susceptibility-induced T2 relaxation, T2 shortening disappears.

Methemoglobin freely diffuses in the hematoma cavity in a locally homogeneous magnetic field. This pattern lengthens T2 and, hence, increases the signal intensity on T2-weighted imaging. Extracellular methemoglobin further enhances T1 relaxation, which manifests as high signal intensity on T1-weighted images. [2, 15]

One study showed that the double inversion recovery sequence has a higher sensitivity for the detection of subacute SAH than CT, 2D or 3D FLAIR, 2D T2*, and susceptibility weighted imaging (SWI). The diagnosis of subacute subarachnoid hemorrhage is important because rebleeding may occur with subsequent life-threatening hemorrhage. This prospective study included 25 patients with a CT-proved acute SAH. [18]

Over months, the hematoma enters the chronic phase. As methemoglobin is broken down into small degradation products, its shortening effects are lost. The degree of hyperintensity on T1- and T2-weighted images lessens as the concentration of methemoglobin decreases with protein breakdown.

The center of the hematoma may evolve into a fluid-filled cavity with signal intensity characteristics identical to those of CSF. In addition, the walls of the cavity may collapse, leaving a thin slit.

As proteins are degraded, iron atoms that are liberated from the heme molecule are scavenged by macrophages and converted into ferritin, which can be recycled. In most cases, the degree of iron deposition overwhelms the recycling capacity, and the excess is locally concentrated into hemosiderin molecules. The iron in hemosiderin does not have access to water protons and, therefore, exerts only a susceptibility effect without notable dipole-dipole interactions. These processes lead to marked hypointensity seen at the rim of the hematoma on T2-weighted MRIs. This appearance may persist indefinitely. [2]

Table 3 (see below) summarizes the evolution of intraparenchymal hematoma.

Table 3. Evolution of Intraparenchymal Hematoma (Open Table in a new window)

Phase

Time

Hemoglobin, Location

Appearance

T1-Weighted MRI

T2-Weighted MRI

Hyperacute

< 24 h

Oxyhemoglobin, intracellular

Isointense or hypointense

Hyperintense

Acute

1-3 d

Deoxyhemoglobin, intracellular

Hypointense

Hypointense

Early subacute

>3 d

Methemoglobin, intracellular

Hyperintense

Hypointense

Late subacute

>7 d

Methemoglobin, extracellular

Hyperintense

Hyperintense

Chronic

>14 d

Ferritin and hemosiderin, extracellular

Hypointense

Hypointense

 

Like parenchymal hemorrhage, subdural hematoma (SDH) has 5 distinct stages of evolution and, therefore, 5 appearances on MRI (see the image below). [19, 20, 21]

Because the dura is well vascularized and because oxygen tension remains high, progression from one stage to another is slower in the lesion than in the brain. The first 4 stages are the same as those for parenchymal hematoma, with the same T1 and T2 characteristics. The chronic stage is characterized by continued oxidative denaturation of methemoglobin, which leads to the formation of nonparamagnetic hemochromates. Also, no hemosiderin rim is seen in the surrounding hematoma and no tissue macrophages are present.

When recurrent bleeding occurs in SDH, separate events can be distinguished by different signal intensities on MRI.

Epidural hematomas (EDHs) evolve in manner similar to that of SDHs. EDHs are differentiated from SDH on the basis of their classic biconvexity versus medially concavity and on the basis of the intensity of the fibrous dura matter. [19]

Subarachnoid hemorrhage (SAH) and intraventricular hemorrhage (IVH) differ from intraparenchymal hemorrhage, subdural hematoma (SDH), and epidural hematoma (EDH) in that they are mixed with CSF. Like EDHs and SDHs, SAHs have high oxygen levels; therefore, they age more slowly than parenchymal hematomas do. (See the images below.)

Immediately after SAH, T1 slightly decreases. This change reflects the increase in the hydration layer due to the elevated protein content of the bloody CSF. This process subtly increases signal intensity in the CSF on T1-weighted images. [22, 21, 3] As in vitro studies have shown, substantial quantities of methemoglobin do not form until several days after hemorrhage has occurred. [22] Several days to a week after the episode, signal intensity increases in the subarachnoid space due to methemoglobin formation.

In cases of mild SAH, RBCs may be resorbed by the time notable methemoglobin formation occurs. Therefore, T1 shortening is seldom seen. For this reason, CT is advocated for the early diagnosis of SAH. [22, 19]

A short-T2 appearance is observed with an SAH or IVH when massive bleeding occurs. In this case, a fluid-fluid level or a subarachnoid or intraventricular thrombus may be present. [22, 3] In chronic and repeated SAH, hemosiderin may stain the leptomeninges, leading to a short-T2 appearance known as superficial siderosis.

Fluid-attenuated inversion recovery (FLAIR) is the most sensitive MRI pulse sequence for detecting SAH. On FLAIR images, SAH appears as high signal intensity (white) compared with normally hypointense (black) CSF spaces. FLAIR MRI is similar to CT in terms of its findings in SAH. T2- and T2*-weighted images can potentially demonstrate SAH as an area of low signal intensity in normally hyperintense subarachnoid spaces. On T1-weighted images, acute SAH may appear as intermediate or high signal intensity in the subarachnoid space. FLAIR images can help in differentiating acute SAH from chronic SAH. [23, 24, 25]

Magnetic resonance angiography (MRA) may be useful in the evaluation of aneurysms and other vascular lesions that cause SAH. Factors that limit the utility of MRI in the diagnosis of acute SAH are its low sensitivity for aneurysms less than 5 mm, its inability to depict small aneurysm contour irregularities, and its difficulty in providing high-quality images in patients who are agitated or confused. MRI, CTA, and angiography may be adequate for identifying and characterizing lesions to enable early surgery to manage ruptured intracranial aneurysms without a need for intra-arterial digital subtraction angiography in the acute phase of the illness.

Primary IVH is rare. It is associated with hypertension, rupture of an aneurysm in the anterior communicating artery, anticoagulation, vascular malformation, moyamoya disease, and intraventricular tumors.

According to one study, MRI identifies small volumes of IVH in cases not detected by CT and yields higher estimates of intraventricular blood volume. The study data indicated that consideration of technical differences is needed when comparing images from the 2 modalities in the evaluation for IVH. CT failed to detect IVH in 3% of cases, whereas MRI was 100% sensitive. MRI and CT yielded equal Graeb scores in 72% of the pairs, and MRI Graeb score was higher in 24%. [7]

MRI has been shown to increase the identification of cerebral infarction inn SAH. In a study of 123 patients with SAH who underwent MRI, 64 demonstrated acute cerebral infarction. Most of the infarcts that were detected on MRI (39 of 64) were not visible on CT. [4]

In a retrospective analysis of patients with SAH undergoing diffusion-weighted MR imaging within 72 hours of onset, age-adjusted ADC (apparent diffusion coefficient) values were globally increased in patients with SAH compared with controls, even in normal-appearing regions, suggesting diffuse vasogenic edema. Cytotoxic edema was also present in patients with SAH and correlated with more severe early injury. [26]

 

Hypertensive hemorrhage is the most common cause of intracranial hemorrhage (ICH). Hypertensive hemorrhage leads to degenerative cerebral microangiopathy characterized by hyalinization of the walls of small arteries and arterioles and, ultimately, fibrinoid necrosis. Because of hypertension, ICH most commonly involves the lenticulostriate arterial branches of the middle cerebral artery, leading to putaminal or caudate hemorrhage. [27] It may also result from rupture of the small perforating branches, in which case it leads to pontine or thalamic bleeds. Large hematomas often dissect into the ventricles, causing intraventricular extension.

Infarcted brain tissue has a propensity to bleed, particularly when reperfused in the acute phase. Hemorrhage due to brain infarction may be recognized because of the associated cytotoxic edema that conforms to an arterial territory. However, this association may be difficult to diagnose when early massive bleeding obscures the underlying infarct. The risk of venous infarction is higher with bleeding than with arterial infarction

Blood from a ruptured saccular aneurysm enters the subarachnoid space. If it is under great pressure, it occasionally dissects into the brain parenchyma. The locations most commonly involved are the medial frontal lobe adjacent to a ruptured anterior communicating artery or anterior communicating artery or an aneurysm of the anterior cerebral artery and the temporal lobes adjacent to a ruptured aneurysm of the middle cerebral artery.

Vascular malformations, such as arteriovenous malformations (AVMs), arteriovenous dural fistulae, and cavernous malformations, can manifest with brain hemorrhage. Both venous angiomas and capillary telangiectasias are generally benign lesions and generally not associated with hemorrhage.

Catheter angiography is often needed to further evaluate AVMs and arteriovenous dural fistula. On MRI, AVM appears as a tightly packed honeycomb of flow voids caused by high-velocity signal loss. Areas of increased signal intensity may be due to slow or turbulent flow or thrombosis. Also seen are areas of hemorrhages in different stages.

Cavernous hemangiomas have a typical popcorn-like pattern with a well-delineated complex and reticulated core of mixed signal intensity due to hemorrhage in different phases. Multiple lesions at different locations are seen in 50% of patients with cavernous hemangiomas.

Developmental venous anomalies, formerly known as venous angiomas, appear as a stellate tangle of venous tributaries that drain into a large, sharply delineated vein, which often shows high-velocity signal loss.

Contusions frequently occur in the basal anterior frontal and temporal lobes where the brain is adjacent to the bony floor of the anterior and middle cranial fossae. They may be seen in the cortex ipsilateral or contralateral to the side of injury. Contusions can be multiple, and they may be associated with other evidence of trauma, such as skull fracture, subdural hematoma (SDH), epidural hematoma (EDH), or subgaleal hematoma.

Brain tumors may be associated with significant neovascularity, breakdown of the blood-brain barrier, and an increased risk for hemorrhage. High-grade tumors such as glioblastoma multiforme, and certain metastases (eg, melanoma, renal cell carcinoma, thyroid carcinoma, choriocarcinoma) are more likely to bleed than others. Metastases from lung cancer can also bleed.

MRI appearances are often atypical and complex because blood of differing ages may be present and admixed with abnormal neoplastic tissue. The evolution of changes in MRI signal intensity is often delayed. Vasogenic edema is greater with brain tumors than with primary ICH, and it persists even into the chronic phase of hematoma. Administration of gadolinium-based contrast medium may reveal tumor enhancement.

Cerebral amyloid angiopathy (CAA) is caused by the deposition of beta-amyloid in the arterial media and/or adventitia of small arteries and arterioles in the meninges, cortex, and cerebellum. CAA often causes hemorrhage in the cortex or in the subcortical white matter of the cerebrum or, in rare instances, the cerebellum. Dissection into the subarachnoid space is common, whereas ventricular extension is uncommon. In elderly patients, lobar ICH and multiple microbleeds are highly suggestive of CAA.

Other causes of ICH are vasculitis, moyamoya disease, anticoagulation therapy, and coagulopathies.

MRA is potentially useful for identifying secondary causes of hemorrhage, such as saccular aneurysm or vascular malformation, which may require urgent intervention. [28] The sensitivity of MRA is good for medium-sized vessels but not as good for those distal to the circle of Willis. 3T MRA may be quite useful in this regard. CTA is also quite useful.

Direct signs of dural sinus thrombosis on magnetic resonance venography (MRV) include absence of the typical high-flow signal intensity from a sinus that does not appear aplastic or hypoplastic on single sections from MRA and the frayed appearance of the flow signal from a sinus after recanalization. Indirect signs of dural sinus thrombosis include evidence of the formation of collaterals, unusually prominent flow signal from the deep medullary veins, cerebral hemorrhage, visualization of emissary veins, and signs of increased intracranial pressure.

On MRI, hemorrhage is occasionally confused with other pathologies or conditions that cause hyperintensity on T1-weighted images. Examples are lesions containing fat, protein, calcification, and melanin.

On T1-weighted images, melanotic metastases have hyperintensity similar to that of intracellular and extracellular methemoglobin. However, metastases from melanoma less commonly display susceptibility on gradient recalled-echo images, and they typically show some contrast enhancement.

Lesions containing fat, such as lipomas or dermoids, are also hyperintense on T1-weighted images. Fat appears hypointense on conventional spin-echo T2-weighted images and hyperintense on turbo fast spin-echo T2-weighted images. Use of fat-suppression techniques, such as chemical shift imaging or inversion recovery sequences (eg, short-tau inversion recovery [STIR]) can help differentiate fat from hemorrhage. The presence of a chemical shift artifact may also indicate a fatty lesion.

Hemorrhagic metastases usually show intense contrast enhancement, which is not seen in bland hematomas.

Calcification may mimic hemorrhage, as both result in profound hypointensity on gradient-echo images. However, differences in the morphology and location of the abnormal signal intensity and in the clinical presentation suffice to distinguish the two. CT may also help differentiate these entities.

Finally, the presence of residual gadolinium-based contrast material can mimic hemorrhage.

As hemorrhage evolves, it passes through 5 well-defined and easily identified stages, as seen on MRI. Knowledge of these stages may be useful for dating a single hemorrhagic event or for ascertaining if multiple hemorrhagic events occurred at different times.

Although CT may be more useful than MRI for detecting hyperacute parenchymal hemorrhage or early subarachnoid hemorrhage (SAH) or intraventricular hemorrhage (IVH), MRI is certainly more sensitive after 12-24 hours. MRI is also more specific than CT in determining the age of a hemorrhage. Both T1- and T2-weighted MRIs should be obtained to adequately characterize and stage a hemorrhage.

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Phase

Time

Hemoglobin, Location

Hyperacute

< 24 h

Oxyhemoglobin, intracellular

Acute

1-3 d

Deoxyhemoglobin, intracellular

Early subacute

>3 d

Methemoglobin, intracellular

Late subacute

>7 d

Methemoglobin, extracellular

Chronic

>14 d

Ferritin and hemosiderin, extracellular

Substance

No. of Unpaired Electrons, e

Magnetism

Oxyhemoglobin

0

Diamagnetic

Deoxyhemoglobin

4

Paramagnetic

Methemoglobin

5

Paramagnetic

Hemosiderin

5

Paramagnetic

Ferritin

5

Paramagnetic

Gadolinium

7

Paramagnetic

Phase

Time

Hemoglobin, Location

Appearance

T1-Weighted MRI

T2-Weighted MRI

Hyperacute

< 24 h

Oxyhemoglobin, intracellular

Isointense or hypointense

Hyperintense

Acute

1-3 d

Deoxyhemoglobin, intracellular

Hypointense

Hypointense

Early subacute

>3 d

Methemoglobin, intracellular

Hyperintense

Hypointense

Late subacute

>7 d

Methemoglobin, extracellular

Hyperintense

Hyperintense

Chronic

>14 d

Ferritin and hemosiderin, extracellular

Hypointense

Hypointense

Jitendra L Ashtekar, MBBS, MD Physician, Department of Radiology, Seth GS Medical College and KEM Hospital, India

Disclosure: Nothing to disclose.

Tufail Ahmed Patankar, MBBS, PhD, MSc, FRCR Consulting Interventional Neuroradiologist, Department of Neuroradiology, Leeds General Infirmary, UK

Tufail Ahmed Patankar, MBBS, PhD, MSc, FRCR is a member of the following medical societies: Royal College of Radiologists, British Society of Neuroradiologists

Disclosure: Nothing to disclose.

C Douglas Phillips, MD, FACR Director of Head and Neck Imaging, Division of Neuroradiology, New York-Presbyterian Hospital; Professor of Radiology, Weill Cornell Medical College

C Douglas Phillips, MD, FACR is a member of the following medical societies: American College of Radiology, American Medical Association, American Society of Head and Neck Radiology, American Society of Neuroradiology, Association of University Radiologists, Radiological Society of North America

Disclosure: Nothing to disclose.

L Gill Naul, MD Professor and Head, Department of Radiology, Texas A&M University College of Medicine; Chair, Department of Radiology, Baylor Scott and White Healthcare, Central Division

L Gill Naul, MD is a member of the following medical societies: American College of Radiology, American Medical Association, American Roentgen Ray Society, Radiological Society of North America

Disclosure: Nothing to disclose.

David S Levey, MD Musculoskeletal and Neurospinal Forensic Radiologist; President, David S Levey, MD, PA, San Antonio, Texas

David S Levey, MD is a member of the following medical societies: American Roentgen Ray Society, Bexar County Medical Society, Forensic Expert Witness Association, International Society of Forensic Radiology and Imaging, International Society of Radiology, Technical Advisory Service for Attorneys, Texas Medical Association

Disclosure: Nothing to disclose.

Intracranial Hemorrhage Evaluation with MRI 

Research & References of Intracranial Hemorrhage Evaluation with MRI |A&C Accounting And Tax Services
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