CLINICAL INDICATIONS MRI and CT are both competitive and complimentary. CT performs better in cases of trauma and emergent situations. It provides better bone detail (calcifications) and has high sensitivity for acute hemorrhage. MRI is more sensitive for cerebral infarction, tumor, infections, white matter disease, PML, leukodystrophy, temporal lobe epilepsy, nonhemorrhagic brain contusions and traumatic shear injuries.

Commonly used MRI techniques T1-weighted imaging: CSF has a low signal intensity in relation to brain tissue, contrast enhancement sequence. T2-weighted imaging: CSF has a high signal intensity in relation to brain tissue. FLAIR imaging: CSF is dark and intracelluar edema has high signal. Gradient echo imaging/SWI: has the highest sensitivity in detecting early hemorrhagic changes. Diffusion-weighted imaging: images reflect microscopic random motion of water molecules Perfusion-weighted imaging: hemodynamically weighted MR sequences are based on passage of MR contrast through brain tissue

MRI pulse sequence abbreviations TSE: turbo spin echo SWI: susceptibility weighted imaging STIR: short tau inversion recovery FLAIR: fluid-attenuated inversion recovery GRE: gradient echo sequences FFE: fast field echo MIP: Maximum Intensity Projection FSE: fast spin echo

Classification of T1-Hyperintense Intracranial Lesions according to Lesion Content

Mechanisms of Contrast Material Enhancement Contrast material enhancement in CNS is a combination of two primary processes: intravascular (vascular) enhancement interstitial (extravascular) enhancement

Interstitial enhancement is related to alterations in the permeability of the blood-brain-barrier. Intravascular enhancement is proportional to increases in blood flow or blood volume. Intravascular enhancement may reflect neovascularity, vasodilatation or hyperemia, and shortened transit time or shunting.

Pachymeningeal enhancement occurs adjacent to the inner table of the skull; in the falx within the interhemispheric fissure; and also in the tentorium between the cerebellum, vermis, and occipital lobes. Pure dural enhancement, without pial or subarachnoid involvement, will not fill in the sulci or basilar cisterns.

Pachymeningeal Enhancement Extraaxial pachymeningeal enhancement may arise from various benign or malignant processes, including: transient postoperative changes intracranial hypotension neoplasms such as meningiomas, metastatic disease secondary CNS lymphoma granulomatous disease

Leptomeningeal enhancement Leptomeningeal enhancement. (a) Diagram illustrates the enhancement pattern, which follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. (b) gadolinium-enhanced T1-weighted MRI in a case of carcinomatous meningitis show pia-arachnoid enhancement along the surface of the brain and extending into the subarachnoid spaces between the cerebellar folia. In addition, leptomeningeal enhancement is usually associated with meningitis, which may be bacterial, viral, or fungal. Figure 8a.  Pia-arachnoid leptomeningeal enhancement. (a) Diagram illustrates the enhancement pattern, which follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns. (b, c) Axial contrast-enhanced CT scan (b) and gadolinium-enhanced T1-weighted MR image (c) in a case of carcinomatous meningitis show pia-arachnoid enhancement along the surface of the brain and extending into the subarachnoid spaces between the cerebellar folia.

Figure 11a. Cortical gyral enhancement Figure 11a.  Cortical gyral enhancement. (a) Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex. There is no enhancement of the arachnoid, and none in the subarachnoid space or sulci. (b) Coronal gadolinium-enhanced T1-weighted MR image in a case of herpes encephalitis shows multifocal, intraaxial, curvilinear, cortical gyri-form enhancement that involves both temporal lobes. The enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead).  Cortical gyral enhancement. (a) Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex. There is no enhancement of the arachnoid, and none in the subarachnoid space or sulci. (b) Coronal gadolinium-enhanced T1-weighted MRI in a case of herpes encephalitis shows multifocal, intraaxial, curvilinear, cortical gyri-form enhancement that involves both temporal lobes. The enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead).

Gyral Enhancement Superficial enhancement of the brain parenchyma is usually caused by vascular or inflammatory processes and is only rarely neoplastic. Vascular causes of serpentine (gyral) enhancement include vasodilatation after reperfusion of ischemic brain, the vasodilatation phase of migraine headache, posterior reversible encephalopathy syndrome (PRES), and vasodilatation with seizures. Serpentine enhancement from breakdown of the blood-brain barrier is most often seen in acutely reperfused cerebral infarction, subacute cerebral infarction, PRES, meningitis, and encephalitis. Gyral lesions affecting a single artery territory are often vascular, whereas inflammatory lesions may affect multiple territories. The most common vascular processes affect the middle cerebral artery territory. However, PRES lesions usually localize in the posterior cerebral artery territory.

Subcortical nodular enhancement Subcortical nodular enhancement. Diagram illustrates nodular lesions near the gray matter–white matter junction and one near the deep gray matter. This pattern is typical for metastatic cancer and clot emboli. Because of their typical subcortical location, metastases often manifest with cortical symptoms or seizures while the lesions are small (often <1 cm in diameter). Figure 15.  Subcortical nodular enhancement. Diagram illustrates nodular lesions near the gray matter–white matter junction and one near the deep gray matter. This pattern is typical for metastatic cancer and clot emboli. Because of their typical subcortical location, metastases often manifest with cortical symptoms or seizures while the lesions are small (often <1 cm in diameter).

Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. Diagram illustrates a thin (<10 mm) rim of enhancement, which is usually very smooth along the inner margin; this pattern is characteristic of an abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter. Figure 18.  Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess. Diagram illustrates a thin (<10 mm) rim of enhancement, which is usually very smooth along the inner margin; this pattern is characteristic of an abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter.

Figure 22a. Necrotic ring pattern of high-grade neoplasms Figure 22a.  Necrotic ring pattern of high-grade neoplasms. (a) Diagram illustrates a lesion with an enhanced rim that is very thick medially; the ring is thicker and more irregular than that seen in a typical abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter. (b, c) Glioblastoma multiforme. (b) Axial nonenhanced T2-weighted MR image shows a large heterogeneous mass that displaces the frontal horn of the lateral ventricle. (c) Axial gadolinium-enhanced T1-weighted MR image shows the irregular, heterogeneous ring-enhancing mass. The ring has a characteristically undulating or wavy margin, and its inner aspect is shaggy and irregular. Diagram illustrates a lesion with an enhanced rim that is very thick medially; the ring is thicker and more irregular than that seen in a typical abscess. The lesion is surrounded by a crown of vasogenic edema spreading into the white matter. (b, c) GBM (b) Axial nonenhanced T2-weighted MRI shows a large heterogeneous mass that displaces the frontal horn of the lateral ventricle. (c) Axial gadolinium-enhanced T1-weighted MRI shows the irregular, heterogeneous ring-enhancing mass. The ring has a characteristically undulating or wavy margin, and its inner aspect is shaggy and irregular.

 Open ring pattern. Diagram illustrates a lesion with an incomplete rim (only part of the rim enhances). This appearance may be seen in multiple sclerosis (without mass effect as in this drawing), tumefactive demyelination (with mass effect), and fluid-secreting neoplasms (with associated mass effect and occasionally with surrounding vasogenic edema). Figure 30.  Open ring pattern. Diagram illustrates a lesion with an incomplete rim (only part of the rim enhances). This appearance may be seen in multiple sclerosis (without mass effect as in this drawing), tumefactive demyelination (with mass effect), and fluid-secreting neoplasms (with associated mass effect and occasionally with surrounding vasogenic edema).

Fourth ventricular CSF pulsation artifact in four subjects Fourth ventricular CSF pulsation artifact in four subjects. A–C, FLAIR axial images of three patients show increasing severity of fourth ventricular CSF pulsation artifact with increasing age: grade 0 in a 32-year-old (A); grade 1 in a 43-year-old (B); and grade 2 in a 71-year-old (C). Subarachnoid CSF artifact is also present in the basal cisterns in B and C.D, The fourth ventricular CSF pulsation artifact that was present on the axial FLAIR image (C) is not visible on this sagittal FLAIR image.E, FLAIR axial image of a subject with fourth ventricular CSF pulsation artifact also shows ghost pulsation artifacts (arrows) in the phase-encoding axis (left to right), causing superimposition of hyperintensities on the bilateral cerebellar parenchyma. Fourth ventricular CSF pulsation artifact. A–C, FLAIR axial images of three patients show increasing severity of fourth ventricular CSF pulsation artifact with increasing age: grade 0 in a 32-year-old (A); grade 1 in a 43-year-old (B); and grade 2 in a 71-year-old (C). Subarachnoid CSF artifact is also present in the basal cisterns in B and C.D, The fourth ventricular CSF pulsation artifact that was present on the axial FLAIR image (C) is not visible on this sagittal FLAIR image. E, FLAIR axial image of a subject with fourth ventricular CSF pulsation artifact also shows ghost pulsation artifacts (arrows) in the phase-encoding axis (left to right), causing superimposition of hyperintensities on the bilateral cerebellar parenchyma.

Diffusion-weighted imaging DWI is sensitive to the microscopic random motion of the water molecule protons, a value known as the apparent diffusion coefficient (ADC), which is measured and captured by this type of imaging. The water molecules move in the direction of the magnetic field gradient; they accumulate a phase shift in their transverse magnetization relative to that of a stationary one, and this phase shift is directly related to the signal attenuation of the image.

Diffusion-weighted imaging ADCs in ischemic areas are lower by 50% or more than those of normal brain areas, and they appear as bright areas (ie, hyperintensities) on the DWI Changes in the ADC occur as early as 10 minutes following onset of ischemia result in intracellular accumulation of water (ie, cytotoxic edema).

MRI in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: Apparent diffusion coefficient (ADC) map obtained from the same patient at the same time.

ADC Cytotoxic edema appears following sodium/potassium pump failure, which results from energy metabolism failure due to ischemic insult; this occurs within minutes of the onset of ischemia and produces an increase in brain tissue water of up to 3-5%. Reduction in intracellular and extracellular water molecule movement is the presumed explanation for the drop in ADC values.

In the acute phase T2WI will be normal, but in time the infarcted area will become hyperintense. The hyperintensity on T2WI reaches its maximum between 7 and 30 days. After this it starts to fade. DWI is already positive in the acute phase and then becomes more bright with a maximum at 7 days. DWI in brain infarction will be positive for approximately for 3 weeks after onset (in spinal cord infarction DWI is only positive for one week!). ADC will be of low signal intensity with a maximum at 24 hours and then will increase in signal intensity and finally becomes bright in the chronic stage. Signal intensities on T2WI and DWI in time

Perfusion-weighted imaging With this technique, information about the perfusion status of the brain is available. The most commonly used technique is bolus-contrast tracking. The imaging is based on the monitoring of a non-diffusible contrast material (gadolinium) passing through brain tissue. The signal intensity declines as contrast material passes through the infarcted area and returns to normal as it exits this area. A curve is derived from this tracing data (ie, signal washout curve), which represents and estimates the cerebral blood volume (CBV).

The diffusion-perfusion mismatch, ie, the difference in size between lesions captured by DWI and PWI, usually represents the ischemic penumbra, which is the region of incomplete ischemia that lies next to the core of the infarction. The ischemic penumbra is regarded as an area that is viable but under ischemic threat; it can be saved if appropriate intervention is promptly instituted. The viability of this region could extend up to 48 hours after the onset of stroke.

Diffusion in yellow. Perfusion in red. Mismatch in blue is penumbra.

A: Hypertensive cerebral angiopathy B: Diffuse axonal Injury C: Cerebral amyloid angiopathy D: CADASIL

Figure 13.  Hypertension-related microhemorrhages in a 91-year-old woman with hypertension and unsteadiness. Axial GRE MR image shows multiple small foci of hemosiderin in both basal ganglia and thalami, locations more consistent with a hypertensive cause. Hypertension-related microhemorrhages. Axial GRE MR image shows multiple small foci of hemosiderin in both basal ganglia and thalami, locations more consistent with a hypertensive cause. Microhemorrhage is not specific for CAA, location, location, location!!!

FLAIR FLAIR + Gd PD/T2 DWI/ADC • Standard sequence for lesion detection, especially in white matter • Less sensitive in the posterior fossa • Usually applied in axial and/or coronal imaging planes • Sagittal FLAIR is indicated in demyelinating disease • Often combined with fat saturation to avoid the “glare” of bright subcutaneous fat FLAIR + Gd • Indicated for the detection of leptomeningeal disease PD/T2 • Proton density (first echo) can be used as an alternative to FLAIR, and is more sensitive for the detection of posterior fossa lesions • T2-WI (second echo) are a staple sequence for detection of long T2 lesions DWI/ADC • Is mandatory in all patients referred with a suspicion of stroke or cerebrovascular disease • Is indicated in the evaluation of cystic lesions (e.g., to differentiate abscess from necrotic tumor, or epidermoid from arachnoid cyst) • Is useful in trauma to detect diffuse axonal injury (DAI) and hemorrhagic lesions.

SWI T1±Gd • Sequence which combines magnitude and phase information • Useful for the detection of intracranial calcifications or hemosiderin deposits (cavernous malformations, hemosiderin deposits, DAI, …) • Is more sensitive for the detection of “microbleeds” than gradient echo T2*-WI T2* • Gradient echo sequence provides information about hemoglobin breakdown products and calcifications • Sensitivity to susceptibility effects is proportional to TE and field strength SWI phase image: Ca++ is bright T1±Gd • Part of most routine brain imaging protocols • Usually applied in sagittal, axial or coronal imaging planes, depending on indication • Same imaging plane should be used before and after gadolinium-chelate injection

Contrast-enhanced MRA MP-RAGE, 3D SPGR (±Gd) • Isotropic 3D T1-W sequence, allowing reformatting in other imaging planes • Provides excellent differentiation between gray and white matter • Indicated to detect migration disorders (e.g., gray matter heterotopia, etc.) • Less sensitive to enhancement as compared to SE or TSE T1-W sequences Fat-sat T2, STIR • Indicated to detect white matter-lesions in “difficult areas,” e.g., in the optic nerve (optic neuritis) TOF MRA • Indicated to examine intracranial vessels and circle of Willis Contrast-enhanced MRA • Indicated in follow-up after endovascular aneurysm coiling • Allows for time-resolved angiography (separating afferent arteries and draining veins)

A 40-year-old female with headache. Review the MR study below. What other MR sequence would be helpful to definitively establish the diagnosis? A: MRA of the circle of Willis diffusion B: Gradient echo C: Fat-saturated image D: Diffusion-weighted imaging

Review the diffusion-weighted image below Review the diffusion-weighted image below. What is the MOST likely diagnosis? A: Dandy-Walker malformation B: Epidermoid C: Ependymoma D: Medulloblastoma (PNET-MB) E: Arachnoid cyst

Epidermoid Epidermoids, like arachnoid cysts, follow CSF on T1- and T2-weighted sequences.  Epidermoids are separated from arachnoid cysts on DWI. Epidermoids commonly occur in the CP angle and are relatively slow-growing.