Neuroimaging
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Neuroimaging
Astrocytomas
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Neuroradiologic evaluation of a patient suspected of harbouring a central nervous system neoplasm has advanced remarkably thanks to the development of computer-based neuroimaging techniques, including computed tomography (CT) and magnetic resonance imaging (MRI). These techniques are now used routinely in the initial evaluation of cranial masses and has resulted in better detection and characterization of intracerebral tumors. Their application has also improved treatment planning through increased accuracy for defining extent of tumor. Postoperatively these imaging modalities are invaluable for delineating the extent of resection of a mass, for early detection of postsurgical complications, for detection of tumor recurrence, and for following the response of a tumor to radiation and chemotherapy.

CT and MRI exquisitely define normal and pathologic intracranial anatomy in a living patient. However, these two techniques use fundamentally different physical principles to image the brain and therefore each provides different and unique information. CT uses differences in x-ray attenuation, which is a function of relative differences in electron density of tissues, to reconstruct a cross-sectional image of the brain. CT is therefore very sensitive to even small amounts of calcium and is also very sensitive for detection of acute hemorrhage, due to the increased density of acute clot relative to nonclotted blood.

MRI, on the other hand, uses differences in the chemical environment of hydrogen in water molecules to image cerebral anatomy. Different pulse sequences are used to emphasize different properties of the regional tissue environment. Because MRI is based on both the amount of water contained in the tissue and the interaction of the water protons with their regional chemical environment, it provides more sensitive detection of tissue differences and more exquisite detail of abnormal lesions compared with CT. Normal gray and white matter structures are identified and pathologic tissue is easily distinguishable from normal tissue. MRI can image the brain in axial, coronal, sagittal, and obliquely oriented planes, improving the assessment of tumor size and extent of tumor infiltration into adjacent structures. This is important for initial evaluation and for follow-up studies, in which changes in tumor size or extent could be missed simply because of partial volume effects or differences in patient positioning if imaging were only done in one plane.

Although definition of cortical bone and paranasal sinus anatomy is much better shown with CT, infiltration of the bone marrow space by tumor or infection is better determined using MRI. This is one example where these two techniques provide complementary information, and there are a number of indications when both imaging modalities are required. By using CT and MRI to obtain as much detail about the morphology of a mass as possible and by correlating these imaging findings with our knowledge of the gross pathologic appearance of various tumors, one can often limit the differential diagnostic possibilities to a relatively specific diagnosis. For example, intracerebral edema, a compromised blood-brain barrier, and areas of necrosis and hemorrhage within a mass are all readily seen. Regional vascular anatomy and the patency of dural venous sinuses can also be defined noninvasively using MR angiography (MRA).

These recent spectacular advances in diagnostic neuroimaging techniques are not without limitations. First. neither CT nor MRI provide a precise histologic diagnosis. Considerable overlap among the characteristic morphologic changes associated with various intracranial lesions necessitates surgical biopsy for diagnosis in virtually all cases prior to initiating definitive therapy. Second, CT and MR images both represent computer-generated maps of the distribution of relative tissue electron density or a spatial representation of differences in water proton T1 and T2 relaxation characteristics, respectively. Although significant pathologic abnormalities usually alter these characteristics, in some instances they may not change detectably from normal. If, as may occur with small tumors or with infiltrative gliomas, there is no significant mass effect distorting normal anatomy, the lesion may go undetected. This is more likely to occur with CT than with MRI, because of the greater sensitivity of MRI. Third, artefacts can degrade CT or MR image quality to nondiagnostic levels. Patient motion during CT or MR image acquisition may introduce abnormal bright or dark areas in a normal brain that can simulate a lesion. Alternatively. streak artefacts from motion can render the examination nondiagnostic. This is less frequently a problem for today's rapid CT scanners. but may be a significant problem for MRI, which requires scanning times of between 2 and 10 min per sequence. The radiology, neurosurgery, and anaesthesiology staff as a team must be prepared to provide safe and effective sedation or, if necessary. general anaesthesia to a patient who is otherwise unable to hold completely still.

Diagnosis of Untreated Cerebral Gliomas

   General Principles

The imaging diagnosis of a cerebral neoplasm is based on a combination of abnormal intracerebral density on CT scan or abnormal signal intensity on MRI scan together with anatomic deformity. Regional cerebral structures are displaced or deformed due to mass effect and compression by the tumor. However, in very slowly growing lesions, such as infiltrating, low-grade gliomas, intracerebral mass effects may be minimal or absent. In these cases, anatomic deformities may be very subtle. There are occasional cases in which the neoplasm may present as an area of isodense or nearly isodense mass on CT or, even more rarely, as an area of isointense signal on MRI. In these cases, minimal deformity of white matter structures and ventricular shift may be the only clues to the presence and location of the tumor.

The imaging appearance of adult cerebral gliomas may be divided into three different patterns. Most commonly, cerebral gliomas appear as areas of diminished attenuation on CT scan or as areas of homogeneously diminished signal on T1-weighted MR images and homogeneously increased signal on T2-weighted MR images. Intracerebral edema has similar characteristics on CT and MRI, respectively, and can be indistinguishable from a nonenhanced infiltrating glioma. The second most common pattern is that of mixed or inhomogeneous changes on CT and MRI. Inhomogeneity is usually due to proteinaceous fluid in necrotic areas or cysts that appear as low-density areas on CT and as areas of low signal on T1-weighted and high signal on T2-weighted images. The least common presentation is a mass of mildly and homogeneously increased density on CT or minimally increased signal intensity relative to gray matter on T1-weighted MR images with minimally hypointense or isointense T2 signal on the T2-weighted images. This last type of appearance is most often seen with hypercellular tumors such as glioblastoma multiforme, lymphoma, or some types of cerebral metastases. When this pattern is present, it is almost always accompanied by a zone of surrounding cerebral edema.

The majority of neoplasms will enhance following the intravenous injection of iodinated contrast material with CT or after the intravenous injection of Gd-based MR contrast material. The areas of enhancement correspond to cellular zones of viable neoplasm containing pathologic neovascularity and endothelial proliferation. Lesions that exhibit contrast enhancement can be localized more precisely. Enhancement is of particular value in tumors that present as homogeneous low-density masses on noncontrast CT or as high-signal lesions on T2-weighted MRI because they would otherwise be difficult to separate from surrounding edema. Localization of the tumor via contrast enhancement is useful for planning the surgical resection of a tumor and is also useful for determining the most appropriate area of the tumor for stereotactic biopsy prior to definitive treatment. The enhancing portion of a lesion corresponds with the most actively growing portion of the tumor and thus is the site of highest diagnostic yield for biopsy. Tumor infiltration is not limited to the area of contrast enhancement but may extend several centimetres into the surrounding area of non enhancing low density on CT or of high T2 signal on MRI. This surrounding area is frequently referred to as the "edematous" zone but actually represents a combination of intracerebral edema and infiltrating tumor. Sparse tumor cells can even be found beyond this "edematous" area in regions that are normal appearing on CT and MRI. Therefore, radiotherapy planning is based on the enhancing mass combined with the area of T2 signal change on MR, which provides the most accurate method for estimating the extent of tumor infiltration. Studies suggest that a 3 cm margin beyond the T2 abnormality will encompass the area of tumor infiltration in most patients with untreated gliomas.

Morphologic characteristics associated with an intracranial mass lesion are also used in formulating a differential diagnosis. Imaging findings on CT or MRI roughly correlate with the histologic grading of cerebral gliomas. Generally, masses that are sharply marginated, are homogeneous in CT density or MR signal intensity, and show little or no contrast enhancement tend to be low-grade gliomas. Masses that have indistinct margins, are inho­mogeneous in appearance. and demonstrate intense, irregular contrast enhancement tend to be high-grade gliomas. These are generalizations and all of the imaging findings and contrast-enhancing patterns of a lesion must be considered together. Individual cases may differ from the norm. Some low-grade astrocytomas that are primarily infiltrating and histologically benign demonstrate poor margination with the surrounding brain on neuroimaging studies and some rapidly growing malignant glioblastomas may show sharp margination from the surrounding brain.

Dean et al. found the degree of mass effect and the presence of cyst formation or necrosis to be statistically significant positive predictors of tumor grade. Central nonenhancing zones within an enhanced mass suggest areas of necrosis and indicate rapid tumor growth that outstrips the blood supply. This is a manifestation of malignant behaviour and should suggest the diagnosis of glioblastoma. Similarly, areas of hemorrhage within a mass also favour a malignant lesion and are most often seen with glioblastomas or metastases.

Very large zones of edema surrounding an enhancing intra-axial tumor also favour the diagnosis of a malignant lesion and contribute to the mass effect associated with these tumors. A notable exception to this rule is a meningioma, which, although a benign tumor, is often associated with large areas of adjacent edema and mass effect. However, these tumors are readily distinguished from malignant gliomas by their extra-axial location. Low-grade gliomas tend to exhibit an infiltrating pattern resembling edema on neuroimaging studies, but the lack of contrast enhancement and the absence of a large mass effect that generally accompanies large zones of cerebral edema help to distinguish these entities.

Calcification within a tumor usually indicates a slowly growing neoplasm. Calcification can frequently be demonstrated in classic oligodendrogliomas and gangliogliomas and may occasionally be seen in astrocytomas and ependymomas. Modern histologic techniques now use immunochemical staining to demonstrate glial fibrillary acidic protein (GFAP) to make the diagnosis of astrocytoma, so many lesions that in the past would have been diagnosed as astrocytomas by their histologic characteristics are now diagnosed as oligodendroglioma or mixed oligoastrocytoma based upon complete or partial absence of GFAP staining. Thus many tumors now classified as oligodendrogliomas may have imaging characteristics similar to those of low-grade astrocytomas and are usually not associated with gross calcification. A tumor with many of the imaging characteristics of a low-grade astrocytoma, including calcification, but which contains an enhancing area, may be a lesion that started out as a benign glioma but has undergone malignant degeneration with areas that demonstrate aggressive histologic changes of anaplastic astrocytoma or glioblastoma multiforme. In these cases, biopsy of the most aggressive-appearing portions of the mass yields the most accurate diagnosis.

  Low-Grade Astrocytoma

The most common CT pattern of a low-grade astrocytoma is that of a low-density homogeneous mass that is poorly marginated from surrounding edema. On MR studies, the lesion is iso- or hypointense on T1-weighted images and hyperintense on T2­weighted images. They grow slowly and hence their mass effect may be less than expected for the size of the tumor on neuro­imaging studies. They tend to infiltrate widely, preferentially growing along white matter tracts of the brain; these lesions may consist entirely of infiltrative cells without a focal mass. They are not restricted to white matter and these tumors often invade deep gray matter structures or extend to the surface and involve cortical gray matter. They are homogeneous in appearance and do not, as a rule, exhibit areas of necrosis or hemorrhage. Following the injection of a contrast agent, enhancement is rarely seen, and when present, it is usually minimal in intensity and patchy or focal in appearance. Nonenhancement of a tumor implies a hypovascular lesion without neovascularity and with an intact blood-brain barrier. This pattern is seen in most low-grade gliomas.

Low-grade astrocytomas infiltrate readily through the deep white matter of the brain and may cross the midline via the corpus callosum or extend into the brain stem via the cerebral peduncles and pyramidal tracts. These lesions are usually well shown by either CT or MRI studies. However, MRI more precisely demonstrates the extent of tumor infiltration and is thus an essential preoperative study. In addition, there are occasional cases where the low-grade glioma may be isointense or nearly isointense on CT but in which the tumor is readily shown on MRI. Thus, in cases where the neurological symptoms or signs are strongly suggestive of a tumor but in which a CT scan is normal or equivocal, an MRI scan is essential to detect an occult glioma.

In some cases, a low-grade glioma may be associated with a cystic component that is represented by a round, sharply circumscribed area of markedly decreased density on CT scan. On MRI the signal characteristics resemble those of CSF but with some­what brighter signal on T1- and proton density-weighted images because of the elevated protein content of the cyst fluid. These cysts are also frequently associated with either a small, nodular area of enhancement along the wall of the cyst or with a thin, smooth rim of enhancement that completely surrounds the cyst. These lesions are more often seen in posterior fossa tumors of young children. However, these cystic gliomas may be seen in adult patients, usually in the cerebral hemispheres, especially adjacent to the third ventricle. Drainage of the cystic component of the tumor is frequently accompanied by striking relief of symptoms and a marked decrease in mass effect.

The differential diagnosis of low-grade astrocytomas may include a cerebral infarct. Acute infarcts are usually distinguished by a characteristic clinical history with an abrupt onset of symptoms combined with an area of low density on CT or abnormal signal on MRI that conforms to the distribution of a vascular territory. A wedge-shaped lesion that is broad based against the surface of the brain and tapers medially is characteristic of an infarct. An infarct characteristically involves both gray and white matter, which become indistinguishable, unlike astrocytomas, which tend to infiltrate throughout the white matter with only mild involvement of cortex or deep gray matter structures. In some instances, the characteristics of tumor and infarct may overlap and the clinical presentation may not be clear. In these instances, a follow-up CT scan after approximately 5 to 10 days will show a typical evolutionary pattern with a cerebral infarct. Mass effect decreases and a characteristic gyri form pattern of contrast enhancement develops. By contrast, a tumor will show no change in appearance in this short period of time. Differentiation from a chronic infarct with gliosis, which may have signal characteristics similar to those of a tumor, is made by noting focal volume loss, rather than mass effect.

Occasionally, an acute area of demyelination may also present as a low-density lesion within the white matter, accompanied by edema, mass effect, and variable enhancement. White matter diseases are best shown on T2-weighted MR images and such studies should always be obtained and carefully scrutinized prior to biopsy or treatment. Multiple white matter demyelinating plaques establish the diagnosis of multiple sclerosis (MS). If the white matter mass presents as a solitary lesion, differentiation from a cerebral tumor may be impossible. In that instance, differentiation can be made with a delayed MRI if MS is suspected. Over 3 to 6 weeks, a tumor will remain stable, whereas a focus of demyelination will show diminished mass effect and edema together with a decrease in the degree of contrast enhancement.

  Anaplastic Astrocytoma

Anaplastic astrocytoma is an intermediate grade of cerebral astrocytoma. Noncontrast imaging studies show many characteristics similar to those of the low-grade glioma, However, mass effect is usually greater and these lesions are more likely to show inhomogeneity on CT and MRI. Most anaplastic astrocytomas will show moderate to intense contrast enhancement. The pattern of enhancement is usually homogeneous and rounded or oval in appearance. Areas of necrosis or hemorrhage are generally not present. On MRI these tumors may also show areas of abnormal high T2 signal intensity surrounding the contrast enhancing portion of the tumor. This nonenhancing zone of abnormal T2 signal may also extend through the white matter.

These tumors are generally not confused with cerebral infarcts because the enhancement patterns of each are characteristically different. A solitary metastasis may mimic an anaplastic astrocytoma and a solitary demyelinating lesion can occasionally be confused with anaplastic astrocytoma.

  Glioblastoma Multiforme

Glioblastoma multiforme is the most aggressive form of astrocy­toma and often has a distinct neuroimaging appearance. Most often these lesions appear as irregular, inhomogeneous areas of abnormality that are poorly marginated from surrounding brain on noncontrast CT and MR studies. Irregular areas of hyperdensity on CT and hyperintensity on T1-weighted MRI and iso- or hypointensity on T2-weighted MRI may be seen and correspond to histologic areas of closely packed malignant cells. These areas enhance following contrast injection. Glioblastomas demonstrate intense enhancement that is irregular in outline, with a rounded or swirl­like appearance surrounding areas of low density on CT or abnormal signal on T1- and T2-weighted MR images that have the characteristics of proteinaceous fluid, old blood, or both. These nonenhancing areas correspond to necrosis within the tumor mass that is characteristic for glioblastoma multiforme and reflects the malignant behaviour and the rapid growth of the tumor. These tumors also show prominent mass effect and deformity associated with prominent areas of cerebral edema. As discussed previously, these zones of hyperintense T2 signal correspond not only to surrounding intracerebral edema but also to infiltrating, nonenhancing zones of tumor. Rarely, no enhancement is seen with a glioblastoma. However, that is understandable if one realizes that a cerebral tumor is graded according to the most malignant histologic section that is observed. If a mass is largely a low-grade glioma but one small section shows histologically malignant characteristics and a microscopic area of necrosis, then the entire tumor is graded as a malignant glioma. This system of grading is used because the clinical behaviour of the tumor is determined by the most aggressive portion of the lesion.

Areas of obvious or occult hemorrhage are frequently observed in glioblastomas. A haematoma from recent bleeding is hyperdense on CT. On MRI, increased signal on T1-weighted images within the hemorrhagic zone corresponds to methemoglobin from sub­acute hemorrhage. Areas of remote or occult hemorrhage are only recognized on MRI studies. These may be seen either as areas of methemoglobin or as areas of markedly diminished signal on heavily T2-weighted images that correspond to zones of hemosiderin deposition. Occasionally, a malignant tumor may present as an intracerebral haematoma of unknown aetiology. In these cases, it is important to differentiate a hemorrhage associated with a tumor from that caused by hypertension or the rupture of an arteriovenous malformation. The latter conditions will show a homogeneous hemorrhagic zone with the characteristics of acute or sub­acute hemorrhage. Tumoral hemorrhage, on the other hand, is often inhomogeneous with evidence of multiple prior haemorrhages of different ages. Fluid levels may be present within the hemorrhage. Enhancement within or immediately adjacent to the hemor­rhagic area indicates an underlying lesion such as a tumor.

Occasionally, glioblastomas may show a paradoxically sharp margination from the surrounding brain as a result of rapid growth with destruction and displacement of the surrounding parenchyma. The other characteristic changes associated with a malignant glioma are usually present and indicate the correct diagnosis. Thus, there is usually a large inhomogeneous tumor mass with irregular enhancement, zones of central nonenhancing necrosis, and extensive surrounding edema.

The differential diagnosis of glioblastoma multiforme includes other aggressive lesions such as metastasis and brain abscess. A solitary metastatic lesion is usually round or oval and is relatively well marginated from the surrounding brain. A metastasis, like a glioblastoma, may contain a central area of nonenhancement, but the necrotic areas of a glioblastoma usually have a more irregular outline. A metastasis is often accompanied by a large amount of cerebral edema that is excessive relative to the size of the tumor, and metastases are usually multiple. A primary brain tumor with multiple enhancing foci may mimic multiple metastases or multiple inflammatory lesions. However, a pattern of multicentric enhancement with intervening nonenhancing mass (rather than edema) on T2-weighted images favour the diagnosis of a primary tumor. In some cases metastases may be distinguishable from glioblastoma only by histologic examination.

An abscess may also mimic a glioblastoma. Abscesses are usually round, smoothly outlined, thin-walled enhancing lesions with a nonenhancing necrotic center. The wall of an abscess, unlike the rim of most glioblastomas, is usually thin, with a smooth round or oval outline. However, a multiloculated abscess or one with daughter abscesses may have an irregular pattern similar to that of a glioblastoma. Similar to glioblastomas, abscesses also show marked surrounding edema, a large mass effect, and intense contrast enhancement. Occasionally, a glioblastoma or metastasis may present as a solitary round mass with a thin rim of enhancement surrounding a central nonenhancing zone mimicking an abscess. However, invariably a glioblastoma wall will have an irregular, shaggy, or nodular margin that suggests the correct diagnosis.

Rarely, a necrotic or malignant meningioma will mimic an intra-axial mass and will have imaging characteristics indistinguishable from those of a glioblastoma. An enhancing dural tail or hyperostosis in the adjacent calvarium, when present, establishes the diagnosis of meningioma. Angiography to demonstrate meningeal arterial supply is occasionally necessary to establish the correct diagnosis.

  Oligodendroglioma

Oligodendrogliomas are slow-growing tumors that historically have accounted for less than 5 percent of cerebral gliomas. However, current immunocytochemical (ICC) techniques have demonstrated that many tumors with the histologic appearance of astrocytoma will partially or completely lack staining for GFAP, and thus are now diagnosed as mixed oligoastrocytomas or oligodendrogliomas, respectively. Thus, using these newer criteria, the incidence of oligodendrogliomas has increased. Oligodendrogliomas occur most frequently in the centrum semiovale of the cerebral hemispheres and are found predominantly in adults. The most characteristic finding on plain x-ray films and CT scans is the frequent occurrence of prominent, irregular clumps of calcification within the tumor mass. In older series, before. ICC techniques were developed for gliomas, calcification in oligodendrogliomas detectable on plain x-ray films of the skull was seen in approximately 40 to 60 percent of patients. However, with the introduction of ICC with GFAP, a higher percentage of gliomas lacking calcification are diagnosed as oligodendroglioma, rather than astrocytoma. Therefore, the percentage of oligodendrogliomas with detectable calcification on CT or plain x-ray film has decreased. Many imaging characteristics of oligodendroglioma are similar to those of astrocytoma. The tumor is a deep white matter lesion that infiltrates widely, and the degree of aggressiveness of the tumor is reflected by the pattern and degree of contrast enhancement, the amount of mass effect, and the degree of inhomogeneity within the tumor mass. Occasionally, oligodendrogliomas may occur within the cerebral ventricles. These lesions may be confused with central neurocytomas  or intraventricular meningiomas, both of which may also contain intratumoral calcification. An oligodendroglioma may undergo malignant degeneration to a glioblastoma, in which case the tumor takes on the imaging characteristics already described for a glioblastoma. This is most often seen in recurrent tumors.

  Ependymoma

Ependymomas arise from ependymal cells lining the ventricles and are most commonly found in the fourth ventricle in children. Adult ependymomas are less common and occur more often within the cerebral hemispheres, usually within the centrum semiovale or adjacent to the third ventricle. They most often are intraparenchymal rather than intraventricular in adults and are thought to develop from cell rests. Despite their histologically benign nature, adult ependymomas may invade the cerebral parenchyma extensively. They are reported to show calcification, but this is infrequent. Ependymomas usually have low density on CT and the MR signal characteristics are similar to those of other low- or intermediate-grade gliomas. They often enhance to a moderate degree in a homogeneous pattern and are surrounded by a small zone of edema with or without accompanying infiltrating, nonenhancing tumor. When they involve the ventricular spaces, they may metastasize via the CSF, especially following surgical treatment. Spinal cord ependymomas have been associated with occult hemorrhage into the adjacent cord or the CSF, but we have not observed this to be characteristic of cerebral lesions.

  Gliomatosis Cerebri

Gliomatosis cerebri is a rare condition of overgrowth of neoplastic glial cells in varying stages of differentiation that diffusely infiltrate large portions of the brain and spinal cord. The underlying neuronal architecture is preserved. The CT pattern usually suggests an ill-defined or diffuse mass effect involving large areas of the brain. The absence of abnormal CT density precludes localizing the lesion or delineating its extent. MRI is much better at imaging gray and white matter structures and at detecting subtle changes in tissue water. Consequently, MRI better delineates a diffuse, infiltrating central mass with mildly to moderately increased T2 signal that is partly due to infiltration of tumor cells and partly due to the demyelination known to occur with this neoplasm. Diffuse, fairly symmetrical thickening of midline structures may be seen. The optic chiasm, hypothalamus, basal ganglia, thalamus, midbrain, pons, cerebellum, and cerebral white matter may be involved. The neoplastic cells tend to follow perineuronal, perivascular, and subpial distributions, and the pattern of abnormal signal reflects this phenomenon. Contrast enhancement is absent except in rare instances of focal necrosis. It can also be seen in areas of dense tumor infiltration that, if subpial, can mimic leptomeningeal spread.

Another entity to consider with this radiologic presentation is hemimegalencephaly. This is a congenital migration anomaly in which one cerebral hemisphere is markedly larger than the contralateral hemisphere. Abnormal gyral patterns, abnormal formation of the gray matter, and enlargement of the ipsilateral cranial vault are typically seen. Occasionally, abnormal signal within the deep white matter from gliosis is present. This entity is usually diagnosed in childhood. Differentiation of these two conditions may be difficult on CT, but MRI findings are characteristic and readily distinguishable.

  Ganglioglioma

Gangliogliomas are uncommon, slow-growing tumors that have mixed elements consisting of neuronal or ganglion cells and glial cells. These lesions have a predilection for the temporal lobes and the posterior fossa. They are usually low-density masses on CT and they resemble low-grade astrocytomas on noncontrasted MRI. They often have calcification and contain cysts and, despite their slow growth and nonaggressive behaviour, they usually show a mild to moderate degree of contrast enhancement. Gangliogliomas are known to occasionally undergo malignant transformation and when this occurs, degeneration invariably occurs along the glial cell line with development of a glioblastoma rather than along the neuronal or ganglion cell lines.

Postoperative Evaluation of Gliomas

Postoperative changes can be grouped into two categories: immediate postoperative changes, which occur during the first few days following surgery, and delayed changes, which occur weeks to months following treatment. Early postoperative imaging is done for two types of evaluation. The first is to detect postsurgical complications, including excessive swelling, cerebral infarction, acute hemorrhage, extra-axial fluid collections that compress the brain, postoperative infection, and hydrocephalus. CT is the procedure of choice in the first few days following surgery because the important findings are all adequately shown or, in cases such as acute hemorrhage, are better shown with CT than MRI. Furthermore, in the early hours and days following cranial surgery, the patient is less able to tolerate long periods within the bore of the magnet, is potentially unstable, and is often attached to multiple monitoring devices that may not be safely placed and may not properly function within the magnet room.

The second indication for early postoperative evaluation is to determine the extent of tumor resection. In patients who preoperatively had a tumor that enhanced with contrast, a CT examination without and with contrast is used to assess the presence and extent of residual tumor. This information is used to plan the patient's subsequent treatment and to provide a baseline against which to monitor its effectiveness. The patient should be imaged within the first four days following surgery. This interval is based on experimental work in animals which showed that the earliest postoperative CT enhancement within the operative site was not seen until postoperative day 4. Thus, the presence of postoperative contrast enhancement during this early postsurgical period directly correlates with residual, nonresected enhancing tumor.

It is important to recognize that nonenhancing tumor cannot be evaluated in this manner. Most nonenhancing gliomas present as low-density lesions on CT that are inseparable from cerebral edema, which is virtually always present in the postoperative patient.

Subsequent follow-up evaluations occur at intervals typically beginning 3 months after surgery, and are designed to evaluate the patient for growth of residual or recurrent tumor. They are almost always performed with MRI evaluation before and after the administration of a contrast agent. If the patient cannot undergo MRI because of safety-related contraindications or severe claustrophobia, follow-up CT without and with iodinated contrast is done. In many instances, if radiotherapy or chemotherapy or both has been used, shrinkage of the residual tumor compared with prior postoperative scans can be demonstrated. New or enlarging areas of enhancing tumor indicate recurrent or actively growing residual tumor.

Radiographic detection of recurrent glioblastoma may precede or coincide with clinical deterioration. It is detected by enlargement of an area of contrast enhancement, enlargement of an area of perilesional low density on CT, or enlargement of an area of abnormal T2 signal on MRI. Recurrent tumor is almost always contiguous with the prior resection bed. Masses are poorly defined and areas of enhancement correspond with areas of high cellularity. Necrosis may also be seen with recurrent glioblastomas as areas of low density, but denser than CSF, without enhancement. True cysts are not seen in untreated glioblastomas, but may be seen in recurrent tumors. Tumors that were nonenhancing preoperatively are usually slow growing, and enlargement of residual or recurrent tumor is only detected as an increasing area of T2 signal abnormality on MRI scans that are spaced months or even years apart. However, in some cases, tumors that are initially low in grade or nonenhancing may undergo degeneration to a more aggressive tumor and recur as an enhancing high-grade malignant tumor.

Within weeks to months following external-beam radiotherapy, MRI scans of the brain may show increased T2 signal within the white matter corresponding pathologically to areas of demyelination and microscopic necrosis associated with hyalinization and fibrinoid necrosis of arterioles. No enhancement is seen and these changes are usually not accompanied by clinical symptomatology. Two patterns have been described: extensive symmetric abnormality involving all the white matter of the hemispheres including the arcuate fibers, and less extensive disease that is most severe in the periventricular white matter. This second pattern may show asymmetrical or symmetrical distribution and, although the pattern may be patchy or focal, it is more frequently confluent. Ventricular dilatation from deep white matter volume loss may be seen. Periventricular white matter tends to be affected first, with extension to the centrum semiovale. The corpus callosum is typically spared. CT is much less sensitive to these changes than is MRI, as is usually the case with white matter disease. If an abnormality is seen, it is of low density in the involved white matter, with or without volume loss. Recognition of this common postradiation change is important and it should not be confused with recurrent tumor or edema. This pattern of radiation change does not seem to be reversible because no recovery of normal white matter signal has been observed over sequential follow-up examinations.

Radiation necrosis can mimic recurrent tumor clinically, and no CT, MRI, and angiography. This is an important pitfall of which one must be constantly aware when evaluating a patient after treatment. Careful evaluation of sequential postoperative and posttreatment scans will detect the presence of a new and enlarging area of enhancing mass. If such a recurrent mass occurs in the zone of maximum irradiation and radiation necrosis is a consideration in the differential diagnosis, evaluation with a positron emission tomography (PET) scan, if available, or with a single photon emission computed tomography (SPECT) scan using thallium 201 can help establish the diagnosis. An area of abnormal enhancement on MRI or CT indicating blood supply to the lesion and breakdown of the blood-brain barrier, accompanied by a zone of markedly diminished regional metabolism as manifested by a markedly decreased uptake of [18F] fluoro-2-deoxyglucose (FDG) on PET or of thallium 201 on SPECT scanning will help to identify an area of radiation necrosis. Areas of new tumor recurrence or new tumor growth will exhibit not only increased blood supply and breakdown of the blood-brain barrier, but also corresponding areas of increased isotope uptake, indicating hypermetabolism on the nuclear medicine studies.

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Introduction |Imaging | Astrocytomas | Glioblastoma Multiforme | Oligodendrogliomas | Ependymomas | Pilocytic Astrocytomas | Gangliogliomas | Mixed Gliomas | Other Astrocytomas | Surgical treatment | Stereotactic Biopsy | Gliadel Wafers |Results and complications | When to Reoperate? | Colloid cyst

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