With an incidence of 8 per 100,000 population per year, primary brain tumors account for 1.4 % of all malignancies, and the risk increases with age (Table 5.7) (Chamberlain and Kormanik 1998). The WHO classification of brain tumors is the most widely utilized classification scheme (Radner et al. 2002; Rousseau et al. 2008). Last revised in 2007, it classifies primary brain tumors according to their tissue of origin and additionally distinguishes four histologic grades based on biological activity (WHO I-IV). The majority of primary brain tumors are of glial origin. Astrocytomas are the most common gliomas, constituting approx. 60 % of cases. Approx. 65–75 % of astrocytomas are accounted for by higher-grade anaplastic astrocytoma (WHO III) and glioblastoma multiforme (WHO IV).

Clinical symptoms depend on tumor location and size. Brain tumors often present with a focal neurologic deficit or symptoms related to increased intracranial pressure. A seizure may be the initial symptom of a cortical tumor such as low-grade astrocytoma.

Low-grade brain tumors typically have uniform low T1 signal intensity (Fig. 5.7a) and appear bright on T2-weighted or FLAIR images (Pope et al. 2005). As there is usually no diffusion restriction, DWI can help in differentiating a brain tumor from atypical infarction. A small cortical tumor may be difficult to distinguish from posttraumatic gliosis, but the absence of signal voids on susceptibility-weighted images may be helpful in making the distinction. With increasing malignancy, a brain tumor becomes more inhomogeneous on both T1-weighted and T2-weighted images (Fig. 5.7b), and diffusion restriction also occurs (Seo et al. 2008).

Cystic lesions of the pineal region are among the most common incidental findings on cranial MRI, occurring in approx. 10 % of all examinations (Table 5.8) (Costa et al. 2008; Pu et al. 2007). Pineal cystic lesions measuring at least 5 mm should be classified as cysts (Sato and Kubota 2009). Pineal cysts typically have the same signal intensity as CSF on both T1-weighted and T2-weighted images (Fig. 5.8a). Depending on the protein content, the cyst fluid may have high signal intensity on FLAIR images. A benign pineal cyst can be septated and contain calcifications. Even contrast enhancement has been described.

Most pineal cysts are asymptomatic. Occasionally, a large cyst compressing the quadrigeminal plate (Fig. 5.8b, c) may cause Parinaud syndrome or headache due to obstruction of CSF flow.

The most important differential diagnoses are infratentorial arachnoid cyst and cavum veli interpositi. If solid components predominate, the differential diagnosis also includes meningioma originating in the tentorium, falx, or velum interpositum. Primary pineal tumors are extremely rare (<1 % of intracranial tumors).

The anatomy of the sella turcica is complex. With the cavernous sinus adjacent to it, the cranial nerves running through it, and the internal carotid artery lying in close proximity, this rather small region includes many important anatomic structures as well as a variety of tissues, giving rise to a wide spectrum of congenital and acquired lesions. In general, sellar MRI should be performed by acquiring thin-slice T2- and T1-weighted sequences (≤3 mm slice thickness) before and after contrast medium administration. These sequences are usually not included in a whole-body screening protocol, often making it difficult to differentiate sellar lesions on screening datasets.

Pituitary adenoma is the most common intrasellar mass, constituting approx. 10–15 % of all intracranial tumors (Table 5.9) (Rousseau et al. 2008; Glezer et al. 2008). The pituitary gland consists of two major divisions, the adenohypophysis (anterior lobe) and the neurohypophysis (posterior lobe). Adenomas arise in the anterior lobe. The normal pituitary gland is isointense relative to brain on both T1-weighted and T2-weighted images. On sagittal images, the normal size of the pituitary gland is ≤10 mm in women (Donovan and Nesbit 1996; Cox and Elster 1991) and ≤8 mm in men. An increased diameter is normal in pregnant and breast-feeding women. In about half of individuals below 35 years of age, the cranial portion of the pituitary gland has a convex shape (Donovan and Nesbit 1996).

Pituitary adenomas are classified by size and hormonal activity. By definition, a microadenoma is less than 10 mm in diameter, while a macroadenoma is 10 mm or larger (Fig. 5.9a). Based on hormonal activity, a distinction is made between functioning and nonfunctioning tumors (30 % of pituitary adenomas). Most nonfunctioning adenomas are macroadenomas. They typically come to clinical attention due to local mass effect causing bitemporal hemianopia by compressing the optic chiasm or causing paresis of cranial nerves III, IV, and VI by invading the cavernous sinus. Conversely, microadenomas present with symptoms related to excess hormone production.

Pituitary adenomas characteristically have a solid appearance but may also have cystic components or be completely cystic (Fig. 5.9b). The differential diagnosis includes craniopharyngioma, especially when the cyst fluid has high T1 and T2 signal intensity and when the largest portion of the tumor is suprasellar in location (Karavitaki et al. 2008). Other differential diagnostic considerations for intrasellar cystic lesions include Rathke cleft cysts, pars intermedia cysts, epidermoids, and dermoid cysts (Glezer et al. 2008; Noh et al. 2007; Naylor et al. 1995), all of which have high T1 signal intensity and low T2 signal intensity.

Meningiomas are the second most common primary brain tumors after gliomas. With an incidence of approx. 6/100,000 population, meningiomas account for 13–26 % of primary brain tumors (Rousseau et al. 2008). They are most common between the ages of 40 and 70, and they are more common in women than in men (ratio of 3:2 to 2:1) (Table 5.10).

Meningiomas arise from arachnoid cap cells, and, because they attach to the dura, they have a characteristic spherical shape. A less common diffuse type, called en plaque meningioma, grows in a flattened fashion along dural structures. The most frequent sites of occurrence of meningiomas are along the parasagittal convexities, along the falx, and along the sphenoid ridges in the hemispheres, at the skull base – particularly along the olfactory grooves and within the sella or in the parasellar region – and in the posterior cranial fossa (Fig. 5.10). Less commonly, meningiomas extend along the optic nerve or occur in intraventricular location. Up to 15 histologic subtypes are distinguished. Most meningiomas are WHO grade I tumors, and morphologic imaging features usually enable no further differentiation (Niedermayer et al. 1998; Nagar et al. 2008).

Meningiomas have nearly the same signal intensity as the brain on both T1-weighted and T2-weighted images (Grunwald et al. 2007) with approx. 20–25 % containing calcifications in the tumor matrix. Calcifications may be seen as hyperintensities on plain T1-weighted images but are best detected as signal voids on susceptibility-weighted images. Rapid growth may be associated with development of perifocal edema. Slowly growing meningiomas can become very large without any major effect on surrounding brain. Slight enlargement of CSF spaces around a meningioma is common and can serve as an indicator that a mass is extra-axial in location (Grunwald et al. 2007; Bonneville et al. 2007).

The Monro-Kellie doctrine states that the cranial cavity is a closed rigid box (Brazis 2008) and that if any of the three CNS components (brain, CSF, blood) increases in volume, intracranial pressure (ICP) will increase as well, unless there is compensatory reduction in the volume of another component. Pseudotumor cerebri, or idiopathic intracranial hypertension, is characterized by increased ICP in the absence of an intracranial mass lesion and is most commonly seen in obese young women. The incidence is approx. 1/100,000 population/year, increasing to approx. 20/100,000/year in women between ages 20 and 40 whose body mass index (BMI) is more than 20 % above the ideal weight (Ball and Clarke 2006). Typical clinical symptoms are headache in 90–95 % of cases and visual impairment in approx. 65–70 % (Brazis 2008). Visual impairment commonly takes the form of optical sensations that can be elicited by a change in posture or Valsalva maneuver. Headache related to pseudotumor cerebri may be transient or permanent and of varying intensity and must be differentiated from tension headache and migraine. Another symptom is pulsatile tinnitus; if the latter is present, the differential diagnosis includes dural arteriovenous (AV) fistula (Table 5.11).

An increase in ICP causes widening of the external CSF spaces along both optic nerves (Rohr et al. 2008). Widened CSF spaces are well detected on coronal T2-weighted fat-saturated images or axial FLAIR images (Fig. 5.11b, c). Concomitant papilledema can be identified as protrusion of the optic disc and flattening of the posterior sclera on axial T2-weighted images. Finally, there will be enlargement of the suprasellar cistern with protrusion into the sella and compression of the pituitary gland, giving rise to the typical empty sella appearance on sagittal images (Fig. 5.11a).

Hydrocephalus occurs when there is an imbalance between the production and resorption of CSF, which, according to the Monro-Kellie doctrine, results in widening of the cerebral ventricles. The most sensitive imaging sign is dilation of the temporal horns with the posterior horns, which are normally pointed, becoming rounded (Greitz 2004).

Normal pressure hydrocephalus (NPH) is a form of communicating hydrocephalus (Kitagaki et al. 1998) with a prevalence of approx. 0.4 % after age 65. NPH is characterized clinically by the classic triad of dementia, unsteady gate, and urinary incontinence, which may vary in severity (Table 5.12) (Bateman 2008).

MRI demonstrates the typical morphology of communicating hydrocephalus, which is characterized by symmetrical enlargement of the ventricles. The fourth ventricle may be spared and retain its narrow shape (Fig. 5.12a, b). A conspicuous finding is a discrepancy between the width of the internal and external CSF spaces, with the external spaces being narrow, especially in the high frontoparietal region (Fig. 5.12c). T2-weighted and FLAIR images will show cap-shaped areas of high signal intensities in the periventricular brain. Another typical finding in NPH is a conspicuous CSF flow void through the aqueduct on sagittal T2-weighted images (Fig. 5.12d) (Scollato et al. 2009).