Structural Imaging Using Magnetic Resonance Imaging and Computed Tomography

Ganglioglioma and gangliocytoma

Gangliogliomas (WHO grade I or II) are mixed tumors containing both neural and glial elements. Gangliocytomas (WHO grade I) are less common and contain well-differentiated neuronal cells without a glial component. Less commonly, gangliogliomas may exhibit anaplasia within the glial component and are classified as anaplastic ganglioglioma (WHO grade III). A rare type of gangliocytoma, dysplastic gangliocytoma of the cerebellum (also known as Lhermitte-Duclos disease ) exhibits a characteristic “tiger-striped” appearance and is often present in association with Cowden disease, a phakomatosis.

The peak age of onset for gangliogliomas is the second decade. This tumor is usually supratentorial and is most commonly located in the temporal lobe. It is well demarcated, and a cystic component and mural nodule are often observed. Calcification is common.

On MRI ( ), the solid component is usually isointense on T1 and hypo- to hyperintense on T2-weighted images. The cystic component, if present, exhibits CSF signal characteristics. The associated mass effect is variable. With contrast, various enhancement patterns are seen—homogeneous or rim pattern—but no enhancement is also possible.

Pilocytic astrocytomas

Pilocytic astrocytomas have two major groups: juvenile and adult. These tumors are classified as WHO grade I. Juvenile pilocytic astrocytomas are the most common posterior fossa tumors in children. The most common locations are the cerebellum, at the fourth ventricle, third ventricle, temporal lobe, optic chiasm, and hypothalamus ( ). The appearance is often lobulated, and the lesion appears well demarcated on MRI. Hemorrhage and necrosis are uncommon. Areas of calcification may be present. The tumor usually exhibits solid as well as cystic components, with or without a mural nodule. The adult form is usually well circumscribed, often calcified, and typically exhibits a large cyst with a mural nodule. On MRI, the solid portions of the tumor are iso- to hypointense on T1- and iso- to hyperintense on T2-weighted images ( ). The cystic component usually exhibits CSF signal characteristics. The associated edema and mass effect is usually mild, sometimes moderate. With gadolinium, the solid components (including the mural nodule) enhance intensely, but not the cyst, which rarely may show rim enhancement.

Pleomorphic xanthoastrocytoma

Pleomorphic xanthoastrocytoma is a rare variant of astrocytic tumors. It is thought to arise from the subpial astrocytes and typically affects the cerebral cortex and adjacent meninges and may cause erosion of the skull. The most common location is the temporal lobe. It is classified as WHO grade II. It usually occurs in the second and third decades of life, and patients often present with seizures. On MRI ( ) usually a well-circumscribed cystic mass appears in a superficial cortical location. A solid portion or mural nodule is often seen, and the differential diagnosis includes pilocytic astrocytoma and ganglioglioma. The signal characteristics are hypointense or mixed on T1-, and hyperintense or mixed on T2-weighted images. With contrast, the solid portions and sometimes the adjacent meninges enhance. Calcification may be present. There is mild or no mass effect associated with this tumor.

Diffuse astrocytomas

Diffuse astrocytomas are well-differentiated tumors (WHO grade II), usually arising from the fibrillary astrocytes of the white matter. Even though imaging may show a fairly well-defined boundary, these tumors are infiltrative and usually spread beyond their macroscopic border. In 2016 update to the WHO classification of central nervous system (CNS) tumors, astrocytoma is subdivided by the presence of isocitrate dehydrogenase (IDH) mutations, with IDH-mutant tumors carrying better prognoses. Although grade II astrocytoma is a relatively slow-growing tumor, they have a relatively high recurrence rate and an inherent malignant potential to transform into high-grade astrocytoma ( ). Two-thirds of cases are supratentorial ( Fig. 40.17 ). A subgroup of these astrocytomas involves specific regions such as the optic nerves/tracts or the brainstem ( Fig. 40.18 ).

Diffuse astrocytomas are iso- or hypointense on T1-weighted images and hyperintense on T2-weighted images. Expansion of the adjacent cortex may be seen, and mass effect (if present) is generally modest. There is little to no surrounding edema. Diffuse astrocytoma usually do not enhance, however, small ill-defined areas of enhancement are not rare. The appearance of enhancement in a previously nonenhancing tumor is a worrisome sign of progression to higher grades.

Anaplastic astrocytoma

Anaplastic astrocytoma is classified as grade III by the WHO grading system. It represents 25%–30% of gliomas, usually appears between 40 and 60 years of age, and is more common in men. Anaplastic astrocytoma is a diffuse infiltrating tumor that often evolves from a well-differentiated astrocytoma as a result of chromosomal and gene alterations. It is most frequently found in the frontal lobes. On MRI, anaplastic astrocytomas appear as poorly circumscribed heterogeneous tumors, which are iso- to hypointense on T1-weighted and hyperintense on T2-weighted images, with associated hyperintensity in the surrounding white matter representing vasogenic edema. Foci of hemorrhage may be present but not too commonly. There is moderate mass effect associated with the lesions, and, with contrast, a variable degree and pattern of enhancement is noted (diffuse or ringlike). This tumor is highly infiltrative, usually cannot be fully removed by surgery, and the median survival is 3–4 years.

Gliomatosis cerebri was previously considered a distinct entity, but since the 2016 update to the WHO classification of CNS tumors , it is now being considered a growth pattern of many gliomas, most commonly, anaplastic astrocytoma. The glial tumor cells are disseminated throughout the parenchyma and infiltrate large portions of the neuraxis. Macroscopically it appears homogeneous and is seen as enlargement/expansion of the parenchyma; the gray/white matter interface may become blurred, but the architecture is otherwise not altered. Unilateral hemispheric white matter is generally involved first; then the pathology spreads to the contralateral hemisphere through the corpus callosum. Later, the deep gray matter (basal ganglia, thalamus, massa intermedia) may be affected as well. Diffuse tumor infiltration often extends into the brainstem, cerebellum, and even the spinal cord. Histologically, most cases of gliomatosis cerebri are WHO grade III.

The MRI appearance is iso- to hypointense on T1 and hyperintense on T2. Hemorrhage is uncommon, and enhancement is also rare, at least in the early stages ( Fig. 40.19 ). Later, multiple foci of enhancement may appear, signaling more malignant transformation. The imaging appearance is similar to that of autoimmune or infectious encephalitis, including subacute sclerosing panencephalitis, but in these disorders, clinical findings are more pronounced.

Oligodendroglioma

Oligodendroglioma, made up by IDH mutant and 1p/19q codeleted cells, accounts for 5%–10% of all gliomas. It arises from the oligodendroglia that form the myelin sheath of the CNS pathways. Oligodendroglioma occurs most commonly in young and middle-aged adults, with a median age of onset within the fourth to fifth decades and a male predominance of up to 2:1. Seizure is often the presenting symptom. The most common location is the supratentorial hemispheric white matter, and it also involves the cortical mantle. The tumor often has cystic components and at least, microscopically, in 90% of cases also shows calcification. Hemorrhage and necrosis are rare, and the mass effect is not impressive. On MRI ( ) the appearance is heterogeneous, and the tumor is hypo- and isointense on T1 and hyperintense on T2. With gadolinium, the enhancement is variable, usually patchy, and the periphery of the lesion tends to enhance more intensely. Oligodendrogliomas are hypercellular and have been noted to appear hyperintense on diffusion-weighted images ( Fig. 40.20 ).

Glioblastoma

Glioblastoma (GBM), previously known as glioblastoma multiforme, is a highly malignant tumor classified as grade IV by the WHO. It is most common in older adults, usually appearing in the fifth and sixth decades and represents 40%–50% of all primary neoplasms and up to 20% of all intracranial tumors. It is subdivided into two types on the basis of the presence or absence of IDH mutation. It is likely that most of the previously recognized primary GBMs were IDH wild-type, and most of the secondary GBMs (from progression of a previous lower-grade tumor) were IDH mutant. Methylation of the promoter for O[6]-methylguanine-DNA methyltransferase (MGMT), the gene for methylguanine methyltransferase, is well recognized as a favorable prognostic factor in GBM ( ).

Glioblastoma forms a heterogeneous mass exhibiting cystic and necrotic areas and often a hemorrhagic component as well. The most common locations are the frontal and temporal lobes. The tumor is highly infiltrative and has a tendency to spread along larger pathways such as the corpus callosum and invade the other hemisphere, resulting in a characteristic “butterfly” appearance. GBM has also been described to spread along the ventricular surface in the subarachnoid space and may also invade the meninges. There are reported cases of extracranial glioblastoma metastases.

Structural neuroimaging distinguishes between multifocal and multicentric glioblastomas. The term multifocal glioblastoma refers to multiple tumor islands in the brain that arose from a common source via continuous parenchymal spread or meningeal/CSF seeding; therefore, they are all connected, at least microscopically. Multicentric glioblastoma refers to multiple tumors that are present independently, and physical connection between them cannot be proven, implying they are separate de novo occurrences. This is less common, having been noted in 6% of cases.

On MRI ( Fig. 40.21 ) glioblastomas usually exhibit mixed signal intensities on T1- and T2-weighted images. Cystic and necrotic areas are present, appearing as markedly decreased signal on T1-weighted and hyperintensity on T2-weighted images. Mixed hypo- and hyperintense signal changes due to hemorrhage are also seen. The hemorrhagic component can also be well demonstrated by gradient echo sequences or by SWI. The core of the lesion is surrounded by prominent edema, which appears hypointense on T1-weighted and hyperintense on T2-weighted images. Besides edema, the signal changes around the core of the tumor reflect the presence of infiltrating tumor cells and, in treated cases, postsurgical reactive gliosis and/or postirradiation changes. Following administration of gadolinium, intense enhancement is noted, which is inhomogeneous and often ringlike, also including multiple nodular areas of enhancement. The surrounding edema and ringlike enhancement at times makes it difficult to distinguish glioblastoma from cerebral abscess. DWI is helpful in these cases; glioblastomas are hypointense with this technique, whereas abscesses exhibit remarkable hyperintensity on diffusion-weighted images.

Owing to its aggressive growth (the tumor size may double every 10 days) and infiltrative nature, the prognosis for patients with glioblastoma is very poor. Despite surgery, irradiation, and chemotherapy the median survival is 1 year.

Ependymoma

Although ependymomas are primarily extra-axial tumors (within the fourth ventricle), intraparenchymal ependymomas arising from ependymal cell remnants of the hemispheric parenchyma are also well known, so this tumor type is discussed here. Ependymomas comprise 5%–6% of all primary brain tumors; 70% of cases occur in childhood and the first and second decades, and ependymoma is the third most common posterior fossa tumor in children. Ependymomas arise from differentiated ependymal cells, and the most common location (70%) is the fourth ventricle. The tumor is usually well demarcated and is separated from the vermis by a CSF interface. The tumor may be cystic and may contain calcification and hemorrhage but these features are more common in supratentorial ependymomas. It may extrude from the cavity of the fourth ventricle through the foramina of Luschka and Magendie. Spreading via CSF to the spinal canal (drop-metastases) may occur, but on spine imaging ependymoma is more commonly noted to arise from the ependymal lining of the central canal, presenting as an intramedullary spinal cord tumor. A subtype, myxopapillary ependymoma, is almost always restricted to the filum terminale.

Ependymomas are hypo- to isointense on T1-weighted images and iso- to hyperintense on T2-weighted images. With gadolinium, intense enhancement is seen, mostly involving the solid components of the tumor, whereas the cystic components tend to exhibit rim enhancement. The differential diagnosis for infratentorial ependymoma includes medulloblastoma, pilocytic astrocytoma, and choroid plexus papilloma.

Lymphoma

Primary CNS lymphoma (PCNSL) is a non-Hodgkin lymphoma, which in 98% of cases is a B-cell lymphoma. It once accounted for only 1%–2% of all primary brain tumors, but this percentage has been increasing, mostly because of the growing acquired immunodeficiency syndrome (AIDS) population. The peak age of onset is 60 in the immunocompetent population and age 30 in immunocompromised patients. Lesions may occur anywhere within the neuraxis, including the cerebral hemispheres, brainstem, cerebellum, and spinal cord, although the most common location (90% of cases) is supratentorial. PCNSL lesions are highly infiltrative and exhibit a predilection for sites that contact subarachnoid and ependymal surfaces as well as the deep gray nuclei.

The imaging appearance of PCNSL depends on the patient’s immune status. The tumor is hypo- to isointense on T1-weighted and hypo- to slightly hyperintense on T2-weighted images. Contrast enhancement is usually intense. In immunocompetent patients ( ) the lesion is often single and tends to abut the ventricular border ( ), and ring enhancement is uncommon ( Fig. 40.22 ). In immunocompromised patients, usually multiple, often ring-enhancing lesions are seen, which are most commonly located in the PV white matter and the gray/white junction of the lobes of the hemispheres, but the deep central gray matter structures and the posterior fossa may be involved as well. Overall, the imaging appearance appears more malignant in the immunocompromised cases and may be difficult to differentiate from toxoplasmosis. Other components of the differential diagnosis in patients with multiple PCNSL lesions include demyelination, abscesses, neurosarcoidosis, and metastatic disease.

Hemangioblastoma

Hemangioblastomas represent only 1%–2% of all primary brain tumors, but in adults they are the most common type of primary intra-axial tumor of the posterior fossa (cerebellum and medulla). These tumors are WHO grade I, well circumscribed, and exhibit a vascular nodule with a usually larger cystic cavity. On MRI the solid portion is hypo- to isointense on T1 and hyperintense on T2-weighted images. Sometimes hyperintense foci are noted on T1; this is due to occasional lipid deposition or hemorrhage within the tumor. The cystic component is usually hypointense on T1 (but may be hyperintense relative to CSF due to high protein content) and markedly hyperintense on T2. On FLAIR images, the cyst fluid is not completely nulled, resulting in a bright signal, and the nodule is also hyperintense. There is usually mild surrounding edema. With gadolinium, the solid component exhibits intense enhancement. Hemangioblastomas are seen in 50% of patients with von Hippel-Lindau disease, and approximately one-fourth of all hemangioblastomas occur in these patients ( ).

Meningiomas

Meningiomas are the most common primary brain tumors of nonglial origin and make up 15% of all intracranial tumors. The peak age of onset is the fifth decade, and there is a striking female predominance that may be related to the fact that some meningiomas contain estrogen and progesterone receptors. These tumors arise from meningothelial cells. In 1%–9% of cases, multiple tumors are seen. The most common locations are the falx (25%), convexity (20%), sphenoid wing, petrous ridge (15%–20%), olfactory groove (5%–10%), parasellar region (5%–10%), and the posterior fossa (10%). Rarely, an intraventricular location has been reported. Meningiomas often appear as smooth hemispherical or lobular dural-based masses ( Fig. 40.23 ). Calcification is common, seen in at least 20% of these tumors. Meningiomas also often exhibit vascularity. The extra-axial location of the tumor is usually well appreciated owing to a visible CSF interface between tumor and adjacent brain parenchyma. Meningiomas may become malignant, invading the brain and eroding the skull. In such cases, prominent edema may be present in the brain parenchyma, to the extent that the extra-axial nature of the tumor is no longer obvious.

On T1-weighted images, meningiomas are usually iso- to slightly hypointense. The appearance on T2 can be iso-, hypo-, or hyperintense to the gray matter. Although MRI does not reveal the histological subtypes of meningiomas with absolute certainty, there have been observations according to which fibroblastic and transitional meningiomas tend to be iso- to hypointense on T2-weighted images, whereas the meningothelial or angioblastic type is iso- or more hyperintense. Not uncommonly, the skull adjacent to a meningioma will exhibit subtle thickening—a useful diagnostic clue in some cases.

After gadolinium administration, meningiomas typically exhibit intense homogeneous enhancement. A quite typical imaging finding on postcontrast images is the dural tail sign , which refers to the linear extension of enhancement along the dura, beyond the segment on which the tumor is based. Earlier this had been attributed to en plaque extension of the meningioma along these dural segments and was thought to be specific for this type of tumor. However, recently it has been recognized that this imaging appearance is not specific to this situation and may be seen in other tumors, secondary to increased vascularity/hyperperfusion or congestion of the dural vessels after irradiation and as a postsurgical change.

Schwannoma

Schwannomas arise from the Schwann cells of the nerve sheath, and the most commonly affected nerve is the vestibular portion of the vestibulocochlear nerve. They are typically bilateral in neurofibromatosis (NF) type 2. The unilateral form sporadically occurs in non-NF patients, with slight female predominance. Schwannomas typically arise in the intracanalicular segment of the eighth cranial nerve where myelin transitions from central (oligodendroglia) to peripheral (Schwann cell) type. If untreated, the tumor grows toward the internal auditory meatus and eventually bulges into the cerebellopontine angle, where it may deform and displace the brainstem. The intra- and extracanalicular parts of the tumor together result in a mushroom- or ice cream cone–like appearance. The tumor is iso- to hypointense on T1-weighted images and iso- to hyperintense on T2-weighted images. This pattern may be modified by the presence of cystic changes or calcification. Gadolinium administration causes homogeneous enhancement that, together with the performance of axial and coronal thin-slice T2-weighted images, allows for the visualization of even very small intracanalicular schwannomas. For images, refer to the section “Neurofibromatosis.”

Primitive neuroectodermal tumor

Primitive neuroectodermal tumor (PNET) is a collective term that includes several tumors arising from cells that are derived from the neuroectoderm and are in an undifferentiated state. The main tumors that belong to the PNET group are medulloblastomas, esthesioneuroblastomas, and pinealoblastomas. The tumors belonging to the PNET group are fast growing and highly malignant. The most common mode of metastatic spread for PNETs is via CSF pathways, an indication for imaging surveillance of the entire neuraxis when these tumors are suspected.

Medulloblastoma

Medulloblastomas arise from the undifferentiated neuroectodermal cells of the roof of the fourth ventricle (superior or inferior medullary velum, vermis). They represent 25% of all cerebral tumors in children, usually presenting in the first and second decade. The tumor fills the fourth ventricle, extending rostrally toward the aqueduct and caudally to the cisterna magna, frequently resulting in obstructive hydrocephalus. Leptomeningeal and CSF spread may also occur, resulting in spinal drop metastases. Cystic components and necrosis may be present. Calcification is possible. On CT, medulloblastoma typically appears as a heterogeneous, generally hyperdense midline tumor occupying the fourth ventricle, with mass effect and variable contrast enhancement. The MRI signal ( ) is heterogeneous; the tumor is iso- or hypointense on T1 and hypo-, iso-, or hyperintense on T2. Contrast administration induces heterogeneous enhancement ( Fig. 40.24 ). Restricted diffusion may be seen on DWI/ADC ( ). Consistent with its site of origin, indistinct borders between the tumor and the roof of the fourth ventricle may be observed, aiding in the differential diagnosis, which in children includes atypical, rhabdoid-teratoid tumor, brainstem glioma, pilocytic astrocytoma, choroid plexus papilloma, and ependymoma. The adult differential diagnosis includes the latter two entities in addition to metastasis and hemangioblastoma. Medulloblastoma does not tend to extrude via the foramina outside of the fourth ventricle, facilitating differentiation from ependymoma. In children, choroid plexus papilloma is more likely to occur within the lateral ventricle.

Esthesioneuroblastoma

The cells of an esthesioneuroblastoma are derived from olfactory neuroepithelium neurosensory cells: hence its other name, olfactory neuroblastoma . This tumor characteristically extends through the cribriform plate to the anterior cranial fossa, orbit, and paranasal sinuses. Invasion of other intracranial compartments and even of the brain is possible, and spreading via CSF has been described. The signal intensity of the tumor is variable. On MRI, T1-weighted signal is usually isointense relative to gray matter, while the T2-weighted signal varies from iso- to hyperintense ( ). With gadolinium administration, intense, sometimes inhomogeneous enhancement is seen. See eFig. 40.25 for a very advanced case of esthesioneuroblastoma that spread to multiple cranial compartments.

Pineoblastoma

Pineoblastomas are highly cellular tumors that are similar in MRI appearance to pineocytomas. However, they tend to be larger (>3 cm), more heterogeneous, frequently cause hydrocephalus, and also may spread via the CSF. This tumor is isointense to gray matter on T1, with moderate heterogeneous enhancement following administration of gadolinium. Like other PNETs, the hypercellularity of pineoblastoma results in T2-weighted signal that tends to be iso- or hypointense relative to gray matter, and restricted diffusion may also be seen. Cysts within the tumor may appear markedly hyperintense on T2, peripheral edema less so. In cases accompanied by hydrocephalus, FLAIR imaging may reveal uniform hyperintensity in a planar distribution along the margins of the lateral ventricles due to transependymal flow of CSF. Peripheral calcifications or intratumoral hemorrhage will exhibit markedly hypointense signal with blooming artifact on T2∗ (pronounced T2-star ) images. Differential diagnostic considerations include germ cell tumor, pineocytoma, and (uncommonly) metastases.

Other pineal region tumors

Besides pineoblastomas, which histologically belong to the group of PNETs, the pineal gland may also develop tumors of pinealocyte origin (pineocytoma) and germ cell tumors.

Pituitary adenomas

The distinction between micro- and macroadenomas is based on their size: tumors less than 10 mm are microadenomas; the larger tumors are macroadenomas. These tumors may arise from hormone-producing cells, such as prolactinomas or growth hormone–producing adenomas, resulting in characteristic clinical syndromes. Pituitary adenomas are typically hypointense on T1-weighted and hyperintense on T2-weighted images, relative to the surrounding parenchyma. This signal change, however, is not always conspicuous, especially in the case of small microadenomas. Gadolinium administration helps in these cases, when the microadenoma is visualized as relative hypointensity against the background of the normally enhancing gland ( Fig. 40.26 ). Following a delay, this difference in enhancement is often no longer apparent, and if the postcontrast images are obtained in a later phase, a reversal of contrast may be noted. The adenoma takes up contrast in a delayed fashion and is seen as hyperintense against the more hypointense gland from where the contrast has washed out. Sometimes when the signal characteristics are not conspicuous, only alteration of the size and shape of the pituitary gland or shifting of the infundibulum may indicate the presence of a microadenoma. Because of this, it is important to be familiar with the normal range of pituitary gland sizes, which depend on age and gender. In adults, a gland height of more than 9 mm is worrisome. In the younger population, however, different normal values have been established. Before puberty, the normal height is 3–5 mm. At puberty in girls, the gland height may be 10–11 mm and may exhibit an upward convex morphology. In boys at puberty, the height is 6–8 mm, and the upward convex morphology can be normal. The size and shape of the gland may also change during pregnancy: convex morphology may appear, and a gland height of 10 mm is considered normal.

While microadenomas are localized to the sellar region, macroadenomas may become invasive and extend to the suprasellar region and may displace/compress the optic chiasm or even the hypothalamus. Extension to the cavernous sinus is also possible (see eFig. 40.27 ).

Craniopharyngioma

Craniopharyngiomas are believed to originate from the epithelial remnants of the Rathke pouch. This WHO grade I tumor may be encountered in children, and a second peak incidence is in the fifth decade ( ). The most common location is the suprasellar cistern ( Fig. 40.28 ), but intrasellar tumors are also possible. The tumor may cause expansion of the sella or erosion of the dorsum sellae. In the suprasellar region, displacement of the chiasm, the anterior cerebral arteries, or even the hypothalamus is possible. Craniopharyngiomas have both solid and cystic components. Histologically, the more common adamantinomatous and the less common papillary forms are distinguished. The adamantinomatous type frequently exhibits calcification. The MRI signal is heterogeneous. Solid portions are iso- or hypointense on T1, whereas cystic components exhibit variable signal characteristics depending on the amount of protein or the presence of blood products. On T2, the solid and cystic components are sometimes hard to distinguish, as they are both usually hyperintense. Areas of calcification may appear hypointense on T2. In contrast, the solid portions of the tumor exhibit intense enhancement.

Advanced structural neuroimaging for planning of brain tumor surgery

Besides functional MRI, advanced structural MRI techniques are also indispensable tools for brain tumor surgery planning. The goal is to maximize the amount of neoplastic tissue removal and to avoid injury to eloquent cortical structures and neural pathways. DTI is an excellent tool for visualization of the nerve fiber systems within and around neoplasms, helping define the boundaries of the planned surgical procedure. The imaging appearance helps decide whether the signal from a certain fiber system is just displaced or disrupted by the neoplasm. Disruption of the fractional anisotropy and signal of a neural pathway indicates the infiltrative nature of the tumor and predicts injury to the fibers if that particular portion of the tumor is removed. eFig. 40.31 demonstrates a case of an infiltrative anaplastic astrocytoma that infiltrates/disrupts multiple fiber systems. On the other hand, extra-axial/compressive tumors and certain, noninfiltrative intra-axial tumors only displace the adjacent pathways—hence those can be preserved during removal of the lesion.

Acute ischemic stroke

With the introduction of intravenous tissue plasminogen activator (IV tPA) and, later, mechanical thrombectomy in the treatment of acute ischemic stroke, timely diagnosis of an ischemic lesion, determining its location and extent, and demonstrating the amount of tissue at risk has become essential (see Chapter 65, Chapter 68 ). CT imaging remains of great value in the evaluation of acute stroke; it is readily available, and newer CT modalities including CTA and CT perfusion imaging are coming into greater use. The applicability of CT to acute stroke continues to be enhanced by the ever-increasing rapidity with which scans can be acquired, allowing for greater coverage of tissues with thinner slices. The technological advances allowing for rapid acquisition of data have led to 4D imaging, where complete 3D data sets of the brain are serially obtained over very short time intervals, allowing for higher temporal and spatial resolutions in brain perfusion studies of acute ischemic stroke patients.

CT is very useful in detecting hyperdense hemorrhagic lesions as the cause of stroke. Early ischemic stroke, however, may not cause any change on unenhanced CT, making it difficult to determine the extent of the ischemic lesion and the amount of tissue at risk. CT is especially limited in evaluating ischemia in the posterior fossa, owing to streak artifacts at the skull base. Despite these limitations, early signs of acute ischemia on unenhanced CT may be helpful in the first few hours after stroke. CT signs of acute ischemia include blurring of the gray/white junction and effacement of the sulci due to ischemic swelling of the tissues. Blurring of the contours of the deep gray matter structures is of similar significance. In cases of internal carotid artery occlusion, middle cerebral artery main segment (M1) occlusion, or more distal occlusions, intraluminal clot may be seen as a focal hyperdensity, sometimes referred to as a hyperdense middle cerebral artery (MCA), or hyperdense dot sign ( Fig. 40.32 ).

Several MRI modalities, as well as CT perfusion studies, are capable of providing data regarding cerebral ischemia and perfusion to assist in the evaluation for possible thrombolytic therapy very early after symptom onset. DWI with ADC mapping is considered to be the most sensitive method for imaging acute ischemia ( Figs. 40.33–40.36 ). In humans, the hyperintense signal indicating restriction of diffusion is detected within minutes after onset ( ).

Temporal evolution of ischemic stroke on magnetic resonance imaging

Acute stroke

Initially, the hyperintense signal on DWI is caused by decreased water diffusivity due to swelling of the ischemic nerve cells (for the first 5–7 days); then it increasingly results from the abnormal T2 properties of the infarcted tissue (T2 shine-through). For this reason, a reliable estimation of the age of the ischemic lesion is not possible by looking at DWI images alone. Imaging protocols for acute ischemic stroke usually include T1- and T2-weighted fast spin echo images, FLAIR sequences, and DWI with ADC maps. These sequences together confirm the diagnosis of ischemia, determine its extent, and allow for an approximate estimation of the time of onset ( ). On ADC maps, the values decrease initially after the onset of ischemia (i.e., the signal from the affected area becomes progressively more hypointense). This reaches a nadir at 3–5 days but remains significantly low until the seventh day after onset. After this time, the values increase (the signal gets more and more hyperintense) and return to the baseline values in 1–4 weeks (usually in 7–10 days). Therefore, ADC maps are quite useful for the estimation of the age of the lesion: If the signal of the area is hypointense on an ADC map, the lesion is likely less than 7–10 days old. If the area is isointense or hyperintense on the ADC map, the onset was likely more than 7–10 days ago. As already noted, although these signal changes take place on ADC maps, the DWI images remain hyperintense, without noticeable changes of intensity by visual inspection.

On T2-weighted (including FLAIR) images, the signal intensity of the ischemic area is normal in the initial hyperacute stage, increases markedly over the first 4 days, then becomes stable. In a research setting, computing the numerical values of hyperintensity in infarcted tissue on serial T2-weighted scans can demonstrate a consistent sharp signal increase after 36 hours, distinguishing lesions younger or older than 36 hours. This is certainly not possible by visual inspection used in clinical practice.

One purpose of MRI in the evaluation of acute stroke is to determine the extent of irreversible tissue damage and to identify tissue that is at risk but potentially salvageable. The combination of DWI and PWI is frequently used for this purpose ( Fig. 40.37 ). Evaluation is based on the premise that diffusion-weighted images delineate the tissue that suffered permanent damage (although in some cases, restricted diffusion is reversible, corresponding to ischemia without infarction), whereas areas without signal change on DWI but abnormal signal on perfusion-weighted images represent tissue at risk, the so-called ischemic penumbra. If there is a mismatch between the extent of DWI changes and perfusion deficits, the latter being larger, reperfusion treatment with mechanical thrombectomy is justified to salvage the brain tissue at risk up to 24 hours of last known normal ( ). If the extent of diffusion and perfusion abnormalities is similar or the same, the tissue is thought to be irreversibly injured, with no penumbra, and therefore the potential benefit from reperfusion treatment may not be high enough to justify the risk of hemorrhage associated with thrombolytic treatment.

Chronic ischemic stroke (3 weeks and older)

Areas of complete tissue destruction with death not only of neurons but of glia and necrosis of other supporting tissues as well, will eventually appear as cavitary lesions filled with fluid that have signal characteristics identical to CSF: hyperintensity on T2-weighted images and marked hypointensity on T1 images and FLAIR sequences. The region of encephalomalacia is bordered by a glial scar (reactive gliosis) that is hyperintense on T2 and FLAIR images ( Fig. 40.38 ). Although the initial signal changes on DWI frequently predict the final extent of tissue destruction, changes on DWI can also disappear, and the final size of tissue cavitation can be best determined on T1-weighted images, which should be part of every stroke follow-up imaging protocol. Tissue in the margins of the cavitary lesion, and often in other areas of the brain as well, may have undergone extensive neuronal loss resulting only in atrophy but not in signal intensity changes, even on T2-weighted images (partial infarction).

Besides signal changes, chronic ischemic infarcts lead to secondary changes in the brain. Owing to the loss of tissue, ex vacuo enlargement of the adjacent CSF spaces (sulci and adjacent ventricular segments) occurs. Pathways that originate from or pass through the infarcted area undergo wallerian degeneration, which is seen as T2 hyperintense signal change along the course of these pathways ( Fig. 40.39 ). Later, the hyperintensity may resolve, but the loss of pathways may result in volume loss of the structures they pass through (e.g., cerebral peduncle, pons, medullary pyramid), noted as decreased cross-sectional area.

Watershed ischemic stroke

Watershed ischemic stroke involves the border zones between the vascular territories of the major cerebral arteries. Infarcts may be superficial, between the territories of the major branches of the circle of Willis, such as anterior watershed infarcts between the proximal territories of the anterior and middle cerebral arteries (see Fig. 40.36 ) and posterior watershed infarcts between those of the middle and posterior cerebral arteries. Deep border zone infarcts develop between the superficial and deep branches of a cerebral artery.

Bilateral, roughly symmetrical watershed infarcts result from global cerebral hypoperfusion caused by heart failure, hypoxia, or hypoglycemia that tends to damage the border zone regions. In unilateral cases, one of these factors is usually coupled with arterial stenosis or occlusion, which can be evaluated with Magnetic Resonance Angiography (MRA) or CTA of the carotid and vertebral arteries.

Ischemic stroke of thromboembolic origin

Thromboembolic stroke results from occlusion of one or more major cerebral arteries or their branches by a blood clot. The occlusion may be due to in situ thrombus formation or embolization from a distant source. Emboli can be of cardiac origin, but they may also be the result of artery-to-artery embolization, commonly due to carotid or aortic arch atherosclerotic disease. The location of infarctions on CT or MRI can orient as to the source of emboli. Unilateral anterior strokes are often due to embolization from the proximal internal carotid artery, a preferential site for atherosclerotic plaque formation. Likewise, unilateral embolic stroke in the posterior circulation necessitates evaluation of the vertebrobasilar system. It should be kept in mind that in case of the quite common anatomical variant of fetal origin of the posterior cerebral arteries (termed fetal PCA when they are predominantly fed by large posterior communicating arteries, which are variably present and arise from the internal carotids), posterior circulation stroke may result from embolization from the anterior circulation. Multiple, especially bilateral, cortical ischemic strokes almost always suggest an embolic origin. If the strokes are bilateral and/or involve both the anterior and posterior circulation, a more proximal embolic source such as the aortic arch or heart can be suspected. Reperfusion injury is a common phenomenon in embolism, and in this stroke type, hemorrhagic transformation of varying degree is often seen.

Lacunar ischemic stroke

Lacunar ischemic strokes constitute 20%–25% of all strokes and are typically seen in patients with hypertension and diabetes. This stroke type is thought to be due to narrowing and in situ thrombosis of the small, deep-penetrating arteries such as the lenticulostriate arteries. The most common locations include basal ganglia, internal capsule, and thalamus. According to structural imaging criteria, their size is usually less than 15 mm in diameter. Acutely, lacunar infarctions may exhibit restricted diffusion if the resolution of the ADC map is high enough to differentiate such from background signal variation. Chronic lacunes have a smoothly rounded, well-defined appearance. The encephalomalacic core of chronic lacunar infarctions follows CSF signal on all pulse sequences, appearing markedly hyperintense on T2 and hypointense on both T1 and FLAIR. There is often a thin rim of hyperintense signal on FLAIR due to gliosis, which helps differentiate lacunes from large Virchow-Robin spaces ( eFig. 40.40 ).

Arteriolosclerosis (white matter hyperintensity of presumed vascular origin)

Diffuse or patchy T2 hyperintense signal changes in the deep hemispheric and subcortical white matter are probably the most common abnormal findings on MRI in the adult and elderly patient population. The terms microvascular ischemic changes , chronic small vessel disease, or leukoaraiosis are alternatively used to describe these lesions on imaging studies. Their etiology and clinical significance have been debated extensively.

Certain hyperintense signal changes are considered normal incidental findings, with no clinical relevance. A uniformly thin, linear, T2 hyperintensity that has a smooth outer border along the border of the body of the lateral ventricles is often seen in the elderly population and likely represents fluid or gliotic changes in the subependymal zone. It tends to be more pronounced at the tips of the frontal horns (ependymitis granularis). This finding is thought potentially to be due to focal loss of the ependymal lining with gliosis and/or influx of interstitial fluid into these regions.

Patchy signal changes within the white matter of the cerebral hemispheres beyond a relatively low threshold (generally, one white matter hyperintensity per decade of life is felt to fall within the normal range) are pathological and are most commonly of ischemic origin. According to the most accepted hypothesis, these hyperintensities are the result of gradual narrowing or occlusion of the small vessels of the white matter, the diameters of which are less than 200 μm (hence the terms microvascular lesions or small vessel disease ). Pathologically, these lesions are composed of focal demyelination and gliosis. The lumen of the involved vessels is narrow or occluded; their walls may exhibit arteriosclerotic changes and commonly amyloid deposits. On imaging studies, they have a chronic appearance, with diffuse borders and no surrounding edema or evidence of mass effect. They are generally associated with some degree of central atrophy, which tends to worsen with higher lesion loads. The distribution of these lesions changes only very gradually on serial scans, often showing minimal to no significant difference on studies spaced several years apart.

While age by itself can cause such changes, and the incidence of these lesions increases with age in people 40 years or older, there are several other risk factors that can make them more numerous. These include hypertension, diabetes, hypercholesterolemia, and smoking. Indeed, patients with these medical problems are more likely to have an elevated number of ischemic white matter lesions.

Chronic ischemic white matter lesions are hypodense on CT, but MRI is much more sensitive and reveals more extensive lesions ( Fig. 40.41, A ). On MRI, the lesions are hyperintense on T2 and FLAIR sequences. They may or may not be visible as T1 hypointensities. It is possible that only lesions visible on T1-weighted images may be clinically significant. Common locations are the PV and, more commonly, the deep white matter, but subcortical lesions are also common, with sparing of the U-fibers. The lesions can be isolated, scattered, or more confluent, especially in the PV zone. Morphologically, individual lesions generally exhibit indistinct borders with a diffuse “cotton-wool” appearance and range in size from punctate to small. Regions of confluent lesions may appear large and more commonly affect the deep white matter anterior and posterior to the bodies of the lateral ventricles, symmetrically within the parietal and frontal lobes. Deep white matter lesions also often occur in a distribution parallel to the bodies of the lateral ventricles on axial views, with an irregular band-like or “beads-on-string” appearance often separated from the PV lesions by an intervening band of relatively unaffected white matter. Involvement of the external capsules is also characteristic. These patterns of lesion distribution and morphology are often best seen on FLAIR. Contrary to the lesions of multiple sclerosis (MS), microvascular ischemia tends not to involve the temporal lobes or the corpus callosum. Besides the hemispheric white matter, microvascular ischemic lesions often also involve the basis pontis (see Fig. 40.41, B and C , available online).

The clinical significance of ischemic white matter lesions depends on their extent and location. The presence of a few small, scattered, ischemic white matter lesions on T2-weighted images is clinically meaningless, and these are usually considered a normal imaging manifestation of aging. Patients may feel more comfortable with descriptions such as “age spots of the brain” to convey their benign nature when verbally discussing results. More extensive lesions also visible on T1-weighted sequences, however, are more likely to be associated with neurological abnormalities such as abnormal gait, dementia, and incontinence. In ischemic arteriolar encephalopathy or Binswanger disease, there is pronounced, widely distributed, and confluent PV and deep white matter signal change. In more severe cases, the confluent hyperintensity also involves the internal and external capsules or subcortical white matter. Besides confluent lesions, coexisting multiple scattered T2 hyperintensities are also very common. Ischemic white matter lesions are often intermixed with lacunar ischemic strokes and generalized cerebral volume loss is also frequently noted.

eFig. 40.42 illustrates a case where the combination of various vascular pathologies, including large vessel stroke, and multiple lacunar infarcts led to vascular dementia.

Scattered small, nonspecific-appearing, seemingly microvascular white matter hyperintensities have a broader differential diagnosis in the younger patient population. Multiple small T2 hyperintense lesions in the hemispheric white matter can be caused by migraine, trauma, inborn errors of metabolism, vasculitis (including Sjögren syndrome, lupus, Behçet disease, and primary CNS vasculitis), Lyme disease, and MS. Since the MRI appearance of these is nonspecific, clinical correlation is always warranted. In many instances, these white matter lesions are idiopathic, and future serial imaging studies are needed for follow-up.

CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an autosomal dominant inherited vascular disease. Pathologically there is destruction of the smooth muscle cells in the small and medium-sized penetrating arteries, with deposition of osmiophilic material and fibrosis leading to progressive thickening of the arterial wall and narrowing of the lumen. As a result, leukoencephalopathy and multiple ischemic strokes occur. Over 90% of patients have detectable mutations of the NOTCH3 gene, which encodes a transmembrane receptor primarily expressed in arterial smooth muscle cells. On MRI, multiple focal infarcts and T2 hyperintense white matter lesions are seen. The white matter lesions may involve the external capsules and, very characteristically, the anterior temporal lobe white matter in a confluent fashion that includes the subcortical arcuate fibers ( eFig. 40.43 ). This latter finding is helpful for the structural imaging diagnosis and also helps distinguish CADASIL from “sporadic” ischemic arteriosclerotic vascular disease.

Hippocampal sclerosis

Hippocampal sclerosis is a potential typical imaging finding in patients with seizures of temporal lobe origin. Previous history of febrile seizures is quite common. On the affected side, the hippocampus exhibits decreased size and often also abnormal T2 hyperintense signal, which is best appreciated on coronal T2 as well as coronal and axial FLAIR images ( eFig. 40.44 ). The underlying pathology is neuronal loss and gliosis involving the CA1 and CA3 regions of the hippocampus. Ex vacuo enlargement of the adjacent segment of the lateral ventricle temporal horn is also seen. There may be involvement of the hippocampus only, but at times other structures of the mesial temporal lobe are also affected and exhibit T2 hyperintensity. In these cases, mesial temporal sclerosis is a more appropriate term.

Venous occlusion/infarction

Venous infarction may follow the thrombosis of cerebral veins (cortical draining veins and the cerebral deep venous system) or of one or more intracranial venous sinuses. The pathogenesis of venous ischemia/stroke is fundamentally different from arterial strokes. Thrombosis of the efferent channels (veins or sinuses) causes elevation of venous pressure, leading to congestion/dilatation of upstream capillaries and venules. This results in interstitial edema, which makes the area of venous infarction/ischemia hyperintense on T2-weighted and FLAIR pulse sequences. Rupture of the vessels may occur, leading to the frequently observed hemorrhagic component of these lesions, best visualized on susceptibility sensitive sequences. Further changes depend on the severity and duration of venous occlusion. Often the congestion is brief or transient, and the ischemic tissue recovers. In these cases, the sometimes very prominent signal changes can resolve, and no residual deficits will remain. In more severe cases that progress to infarction, restriction of diffusion (hyperintense signal on DWI and hypointense signal on ADC maps) is a common finding due to cytotoxic edema. Cytotoxic and vasogenic edema also results in hypointense signal on T1-weighted images. The venous etiology of the stroke is suggested by the morphological appearance of the lesion. Its distribution does not follow an arterial branch pattern. The appearance of the hyperintense signal changes on T2-weighted images and FLAIR sequences is also different; oftentimes heterogeneous signal changes are noted within the venous infarction, consisting of a “curly cue” or “fudge-swirl” pattern. Tumor-like appearances are also possible.

In cases of ischemia/stroke that are suspected to be of venous origin, it is important to carefully evaluate the draining veins in the area, and the sinuses as well, to look for thrombosis. The normal flow voids on MRI may be absent, replaced in some cases by hyperintense signal changes on FLAIR or hyperdensities on CT that exhibit a tubular or curvilinear string-like morphology. However, the pattern and distribution of cortical draining veins is very variable, which makes it difficult to pinpoint abnormalities of individual veins. Sometimes there is a striking absence of visualizable draining veins. Conversely, in cases of sinus thrombosis, massive engorgement of the veins may be seen. Venous thrombosis frequently starts at the level of a draining vein. In these cases, magnetic resonance venography (MRV) may be initially unremarkable. MRV will become abnormal only later when the thrombosis progresses to the venous sinuses. Suspected cases of venous infarction are often best evaluated with two modalities: conventional MRI or CT in conjunction with MRV or a CT venogram. eFig. 40.45 demonstrates the evolution of a venous infarct, due to left transverse sinus thrombosis, from the acute to chronic stages.

Cerebral venous sinus thrombosis

Acute cerebral venous sinus thrombosis results in diminished or absent flow in the involved sinuses. Cerebral venous sinus thrombosis usually causes typical signal changes on MRI ( Fig. 40.46 ) and severely attenuated or absent flow signal on MRV. MRV techniques include flow-sensitive modalities such as 2D time-of-flight and phase contrast imaging, as well as postcontrast high-resolution three-dimensional spoiled gradient-recalled (3D SPGR), which offers excellent visualization of the sinuses with a very high spatial resolution and contrast-to-noise ratio.

In the appropriate clinical context, a useful sign of venous sinus thrombosis is the absence of a normal hypointense flow void in the involved sinuses on T1- and T2-weighted images and absent flow in the involved sinus on MRV. Nonflowing blood generally results in increased signal intensity on T1 and T2. In the early acute stage, however, the sinuses may still be hypointense. This is followed by signal that is isointense to the gray matter. The typical hyperintense signal on T1- and T2-weighted images appears when methemoglobin is present in the clot. At all stages, therefore, simultaneous review of the MRV or CT angiogram for lack of flow signal and lack of contrast filling in conjunction with conventional MRI may be particularly useful to increase the sensitivity and specificity of detection of sinus thrombosis while also adding information regarding the age of the clot.

Following administration of gadolinium, there may be enhancement of the dural wall of the sinus and along the periphery of the clot, but not within the clot itself, resulting in an “empty delta” appearance. This is classically a CT finding, but the same concept also applies to MRI in the context of the T1-weighted clot signal that varies with clot age. MR demonstrates lack of flow, appearing as absence of contrast-related signal in the involved sinuses. CT angiogram reveals no contrast filling in the thrombosed sinuses. The cortical veins that drain into the involved sinuses may appear engorged on MRV. However, if the thrombosis also involves these draining veins, they too may exhibit lack of signal on MRV, lack of filling on CT angiogram, and lack of flow voids in conjunction with iso- or hyperintense signal on T1- and T2-weighted images.

Variations in the speed of blood flow and anatomical variants of the venous sinuses may change their usual signal characteristics, leading to a false diagnosis of venous sinus thrombosis. Slow flow in a venous sinus may cause increased signal on T1- and T2-weighted images, potentially leading to a false assumption of thrombosis. Gadolinium-enhanced images help in these cases, demonstrating contrast filling/enhancement in the sinuses and confirming the absence of thrombosis. A normal variant of venous sinus hypoplasia/aplasia may result in decreased/absent flow signal on MRV, falsely interpreted as thrombosis. T1- and T2-weighted images, however, are usually able to demonstrate the absence of thrombus in the sinus. These examples highlight the importance of reviewing all necessary image modalities (MRV, T2-weighted images, T1-weighted images with and without contrast) to make or reject a diagnosis of venous sinus thrombosis.

Hyperacute hemorrhage (0–24 hours)

In the early (hyperacute) phase of intraparenchymal hemorrhage (<24 hours) the red blood cells are intact, and a mixture of oxy- and deoxyhemoglobin is present ( ). In this stage, the signal on T1-weighted images is isointense to the brain, so even larger hematomas may be missed on this pulse sequence. On T2-weighted images, the oxyhemoglobin portion is hyperintense and deoxyhemoglobin is hypointense, resulting in the gradual appearance of a hypointense rim and gradually increasing hypointense foci within the hematoma as the amount of deoxyhemoglobin increases from the periphery. Such hypointense foci are also seen on FLAIR. Between the clot and the deoxyhemoglobin-containing rim, thin intervening clefts of fluid-like T2 hyperintensity may be seen as an initial manifestation of clot retraction. On gradient echo images, hyperacute hemorrhage will exhibit heterogeneously isointense to markedly hypointense signals, the latter corresponding to deoxyhemoglobin content in more peripheral portions of the clot. The amount of edema is mild in this stage, usually seen as a thin rim that is hyperintense on T2 and FLAIR images and hypointense on T1-weighted images ( ).

Acute hemorrhage (1–3 days)

During this stage, hemoglobin is transformed to deoxyhemoglobin, but the membranes of the erythrocytes are still intact ( ). The hematoma becomes slightly hypointense on T1 and strikingly hypointense on T2-weighted images ( Fig. 40.47 ). On GRE, proton spins in the presence of paramagnetic deoxyhemoglobin dephase rapidly during TE, resulting in signal loss and, therefore, hypointensity of the hematoma on this pulse sequence. The surrounding edema, which is more extensive during this stage, is hypointense on T1 and hyperintense on T2.

Early subacute hemorrhage (3 days to 1 week)

As blood degradation evolves, deoxyhemoglobin is converted to methemoglobin. At this stage, the blood degradation products are still intracellular ( ). Intracellular methemoglobin is hyperintense on T1 and hypointense on T2-weighted images. T1 shortening is primarily the result of dipole–dipole interactions between heme iron and adjacent water protons, facilitated by a conformational change that occurs when deoxyhemoglobin is converted to methemoglobin.

Signal changes on T2 occur via a different mechanism. Sequestration of methemoglobin within the intact red blood cell membrane results in a locally paramagnetic environment adjacent to the diamagnetic, methemoglobin-free extracellular compartment. These differences in the local magnetic fields, present at a microscopic level, cause rapid dephasing of proton spins and signal loss during TE as water molecules diffuse rapidly through this heterogeneous environment. Therefore, on T2-weighted images, the presence of intracellular methemoglobin results in hypointensity of the hemorrhage. These signal changes start from the periphery of the hematoma where the deoxyhemoglobin-to-methemoglobin transformation first occurs. During this stage, the amount of edema starts to decrease.

Late subacute hemorrhage (1–4 weeks)

In the late subacute phase, the membranes of the red blood cells disintegrate, and methemoglobin becomes extracellular ( ). Extracellular methemoglobin contains Fe ³⁺ , which has five unpaired electrons. This leads to a dipole–dipole interaction that, contrary to intracellular methemoglobin, causes hyperintense signal change on both T1- and T2-weighted images ( Fig. 40.48 ).

During this stage (usually 2 weeks after the hemorrhage) hemosiderin deposition begins, typically at the periphery of the hematoma where macrophages reside. A dark peripheral rim appears on GRE and T2-weighted images, which is initially thin but then progressively thicker. The amount of edema around the hematoma continues to decrease gradually.

Chronic hemorrhage (>4 weeks)

In the chronic stage ( ), the core of larger hematomas turns into a slitlike or linear cavity with CSF signal characteristics, being hypointense on T1 and FLAIR and hyperintense on T2-weighted images. At the periphery of the lesion, macrophages continue to remove iron from the extracellular methemoglobin; hemosiderin and ferritin are deposited in their lysosomes, resulting in a rim of hypointense signal on T2-weighted and GRE images. This hypointense rim becomes progressively more prominent during the transition from the late subacute to chronic stage ( Fig. 40.49 ).

If the hemorrhage is small, eventually its entire area will be occupied by hemosiderin deposition. Smaller hemorrhages or microbleeds, such as those seen in amyloid angiopathy or after head trauma, are visualized as multiple uniformly hypointense foci on GRE images. Susceptibility-weighted images are even more sensitive to magnetic field distortion due to blood products and can reveal microbleeds that are missed even by conventional gradient echo images. It is important to keep in mind that because of magnetic field distortion, the area of hypointensity on GRE or susceptibility-weighted images is larger than the actual size of the bleed. GRE or, ideally, SWI should be part of every MRI protocol for brain trauma.

Hemorrhage, like many other lesions to the brain, provokes reactive gliosis. In the chronic stage, surrounding gliosis is seen as mildly hyperintense signal on T2 and FLAIR images.

Bacterial meningitis

In the typical uncomplicated form of bacterial meningitis, no abnormalities are seen in the brain parenchyma, and without contrast administration, the meninges may also appear unremarkable. With gadolinium, however, intense meningeal enhancement is seen, usually over the convexities and along the basal cisterns; this is due to vascular engorgement and increased vascular permeability secondary to the inflammatory process. At times, as a complication, ventriculitis may develop, and then the ependymal lining of the ventricles also exhibits enhancement.

Cerebritis, abscess

Cerebritis and abscess can arise as complications of bacterial meningitis, but they may also spread to the brain hematogenously from another source such as endocarditis or pulmonary abscess. Cerebritis and abscess refer to different stages of the parenchymal infection. In the cerebritis stage, the lesion has poorly defined hyperintensity on T2 and FLAIR sequences and is iso- to hypointense on T1-weighted images. Foci of necrosis may be present. There is surrounding edema, appearing as hypointensity on T1 and hyperintensity on T2 and FLAIR. With gadolinium, a heterogeneous irregular enhancement pattern may or may not be present.

If the process continues to cerebral abscess formation, after an average of 2 weeks, the core appears more demarcated and fibrotic capsule formation is noted. The center of the abscess contains liquefied, necrotic, and purulent material. This is usually hypointense on T1 (but may appear more hyperintense, depending on the protein content) and hyperintense on T2. The rim is iso- to hypointense on T1 and iso- to hypointense on T2. Often the T2 hypointense rim is well seen, separating the hyperintense core from the usually less hyperintense surrounding edema. With gadolinium, the capsule exhibits ring enhancement, which is typically a smooth, thin, complete ring. Sometimes the deeper segment of the enhancing ring is thinner than the superficial. A characteristic feature that supports the diagnosis of abscess is the so-called daughter abscess, which is seen as a smaller ring-enhancing lesion connected to the parent abscess.

Cerebral abscesses are part of the differential diagnosis when ring-enhancing cerebral lesions are encountered. Besides the described ring morphology and the potential presence of daughter abscesses, cerebral abscesses exhibit restriction of diffusion centrally, appearing as hyperintense signal on diffusion-weighted images and hypointensity on ADC maps, which distinguishes them from metastatic and most primary brain tumors ( eFig. 40.52 ).

Central nervous system tuberculosis

Tuberculosis may involve the brain parenchyma in the form of tuberculomas ( eFig. 40.53 ), cerebritis, or cerebral abscess. Tuberculomas are isointense on T1; the T2 appearance is variable. At times a mildly T1 hyperintense and T2 hypointense rim is seen around them. Tuberculomas exhibit solid or ring enhancement and, similar to tuberculosis-related abscesses, enhance intensely; in cases of ring enhancement, it is usually thicker and more irregular than seen with pyogenic abscesses. In chronic tuberculomas, areas of calcification are sometimes noted. Tuberculous meningitis is another frequent occurrence in this disease, with diffusely abnormal meningeal enhancement being most intense along the basal meninges; distinct nodules may also be noted. Ventriculitis with ependymal enhancement is also possible. Tuberculosis-related vasculitis may complicate the disease, causing infarctions of various sizes.

Lyme disease

In the brain parenchyma, Lyme encephalitis may cause multiple lesions that are slightly hypointense on T1- and hyperintense on T2-weighted images. The most common locations are the subcortical and PV white matter, but the thalamus, corpus callosum, and pons may be involved as well. The lesions appear nonspecific, their size ranging from a few millimeters to a centimeter. Vasculitis, demyelinating disease, and microvascular ischemia are frequent differential diagnostic considerations. If present, abnormal enhancement along the meninges and cranial nerve segments may indicate involvement of these structures by Lyme disease.

Cysticercosis

Among the parasitic infections of the CNS, cysticercosis is the most common. It is caused by the larval form of Taenia solium . The infection may involve the parenchyma, but meningeal, subarachnoid, and intraventricular locations are also common. The lesions are usually cystic, and the cysts often exhibit a T1 hyperintense central scolex. Intraparenchymal cysts are common at the gray/white junction, their size ranging from millimeters to a few centimeters. The cyst itself is of variable signal intensity, hypo- to hyperintense on T1 and iso- to hyperintense on T2. The cyst and its leaking contents provoke an inflammatory reaction in the surrounding parenchyma, resulting in edema and later gliosis, both appearing as T2 hyperintensity. With gadolinium, the amount of enhancement depends on the degree of inflammatory reaction. As the larva dies, the cystic lesion usually retracts, and at the chronic stage there is calcification without contrast enhancement. See eFig. 40.54 for a case, with corresponding gross pathology.