Nonneoplastic Mass Lesions of the Central Nervous System

C H A P T E R

53 Nonneoplastic Mass Lesions of the Central Nervous System S.B. Omay1, K.K. Atsina1, J.M. Baehring1,2 1Department

of Neurosurgery, Yale School of Medicine, New Haven, CT, USA; 2Departments of Neurology and Medicine, Yale School of Medicine, New Haven, CT, USA

Nonneoplastic mass lesions of the central nervous system (CNS) mimic tumors clinically and radiographically; their etiology is diverse. Although nonneoplastic mass lesions may also require surgical resection, recognition of such lesions and an accurate diagnosis utilizing only imaging modalities may, at times, spare the patient from invasive procedures. Failing to differentiate between the two may delay treatment in malignant tumors or result in unnecessary treatment in nonneoplastic lesions.1 When surgery is required, utilization of imaging modalities to accurately predict a diagnosis may help the neurosurgeon plan the intervention accordingly. This chapter provides an overview of nonneoplastic mass lesions and their characteristics on neuroimaging studies.

DEVELOPMENTAL ABNORMALITIES

fluid (CSF) on T1- and T2-weighted images. On fluidattenuated inversion recovery (FLAIR) images, the signal may not be completely suppressed owing to proteinaceous contents. On gadolinium-enhanced images, enhancement of the cyst wall occurs in most pineal cysts but is typically incomplete; this finding has been attributed to fragmentation of the pineal parenchyma as the cyst enlarges. On the other hand, at delayed imaging, uniform enhancement of the cyst has been reported.5 The mechanism behind this finding is not understood, but it may be related to passive diffusion of the contrast agent through the cyst wall or to active secretion of contrast agent by the cyst wall.4 Fine internal septa and internal cysts may be seen at high-resolution imaging. The differential diagnosis includes cystic tumors such as astrocytoma, pineocytoma, and pineoblastoma.6

Pineal cysts

Arachnoid cysts

These lesions are benign cysts composed of an inner layer of gliotic tissue with pineal parenchymal tissue and connective tissue as the outer layer.2 Their incidence (>5 mm) was found to be 2.6% in adults in retrospective magnetic resonance imaging (MRI) studies,3 while other studies reported their prevalence as 25–40% of cases in autopsy series and in 23% of patients in imaging studies of normal volunteers.4 Pineal cysts are usually asymptomatic lesions found incidentally. The majority of these lesions remain stable7 and can be followed by repeat imaging, but rapid enlargement may require histological diagnosis and surgical resolution of the mass effect. On MRI, pineal cysts are round or oval, thin walled, and well circumscribed (Figure 1A). They typically demonstrate signal intensity similar to that of cerebrospinal

Arachnoid cysts are collections of CSF localized with the arachnoid membranes. They are extra-axial by definition. They are more prevalent in males and mostly present in the pediatric population.8 Arachnoid cysts can present in many different locations. Most commonly, they are found within the middle cranial fossa with an incidence of 42% followed by retrocerebellar and convexity locations.8 Depending on location, arachnoid cysts may present with headaches, seizures, and rarely hemorrhage in the cyst. In patients with symptomatic arachnoid cysts, treatment may lead to lasting relief of focal neurological deficits; treatment modalities involve endoscopic or open fenestration and shunt placement.8,9 Arachnoid cysts present as extra-axial masses, they are well circumscribed and cause calvarial remodeling.

Handbook of Neuro-Oncology Neuroimaging, Second Edition http://dx.doi.org/10.1016/B978-0-12-800945-1.00053-7

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FIGURE 1A  Developmental mass lesions. (a) Pineal cyst (arrowhead). There is flattening of the quadrigeminal plate. The cyst wall is regular and does not enhance (T1W with gadolinium). (b) Arachnoid cyst (arrowheads). There is mass effect on the cerebellum (T1W with gadolinium). (c) Colloid cyst (arrowhead). Cyst content is slightly hyperintense compared to normal white matter (T1W).

They follow CSF density and intensity in computed tomography (CT) and MRI, respectively. They do not enhance with contrast. Diffusion-weighted imaging fails to reveal restriction of water diffusion, which helps differentiate arachnoid cysts from epidermoid tumors.10

Epidermoid Cysts Epidermoid cysts are developmental lesions believed to arise from midline ectodermal cells that are displaced during embryogenesis, or from multipotent embryonic cells or displaced otic capsule cells (for those arising in the cerebellopontine angle (CPA)). They tend to occur off midline and are most commonly found in the CPA as well as the petrous apex and in the parasellar area.11–13 Clinical presentation is dependent on location: CPA lesions present with symptoms of hearing loss, tinnitus, and sometimes trigeminal neuralgia; parasellar lesions cause headache and visual symptoms. Although technically difficult owing to adhesions to neighboring neurovascular structures, total excision is the recommended treatment for these lesions. They are likely to recur in subtotally resected cases.11 Pathologically they are composed of keratinized squamous epithelium. Although rare, secondary development of squamous carcinoma has been reported.14 On imaging studies, epidermoids tend to be hypodense on CT and may show calcification. They follow CSF intensity on MRI with T1-weighted (T1W) hypointensity and T2W hyperintensity, but FLAIR signal suppression is incomplete. Perilesional edema is uncommon. Typically there is no enhancement. Lesional margins may be irregular. Characteristically they show restricted diffusion of water.15,16

Dermoid Cysts Dermoid cysts are also developmental lesions containing dermal elements like hair, hair follicles, or sweat glands. They are rarer compared to epidermoid cysts, constituting about 0.05% of all brain masses.17 They tend to occur in younger patients with an average age of 15 years.18 In contrast to epidermoid cysts, which contain keratin and epithelial cell debris, dermoid cysts contain elements of the dermis including hair, hair follicles, dental enamel, sweat glands, and sebaceous and apocrine glands.16 Dermoids tend to be closer to the midline, with the vermian and parasellar regions as the most common sites of presentation. Treatment of these lesions is surgical. Incomplete resection leads to recurrence many years later as these lesions tend to grow indolently. On CT imaging, dermoids appear as a well-defined hypodense mass (Figure 1B). Calcifications are common. On MRI, they are hyperintense on T1W imaging and heterogeneous on T2W sequences.10

Neuroenteric Cysts Neuroenteric or neuroepithelial cysts are developmental malformations. Most commonly encountered locations are the spinal column, pontomedullary junction, CPA, craniocerebral junction, and parasellar area.19 They are mostly localized ventrally and extra-axial within the spinal column. Spinal neuroenteric cysts are associated with vertebral anomalies such as hemivertebrae, fused vertebrae, or diastematomyelia and more complex syndromes such as Klippel–Feil syndrome. The cyst wall usually is composed of cuboidal, columnar, or ciliated epithelium, with or without goblet cells or microvilli resembling gastrointestinal epithelium. Symptoms

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Developmental Abnormalities

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FIGURE 1B  Developmental mass lesions. (a) Dermoid cyst. A large hyperintense lesion expands the pituitary fossa and extends into the base of frontal lobe and hypothalamus (T1W). (b) Epidermoid cyst. A large mass with a cauliflower-like appearance compresses the tectum of the midbrain. There is restriction of water diffusion (DWI). (c) Lipoma of the thoracic spinal cord. A large hyperintense mass lesion is seen within the center of the cord. It appears to be tethered to the posterior dura at its caudal end (T1W).

are related to location and most commonly related to mass effect.20 Surgery is usually reserved for symptomatic lesions. The goal is for complete cyst wall resection, except in situations of adherence to critical structures. For complex, unresectable cysts, shunting into the subarachnoid space may be considered. MRI signal intensity varies with the cyst contents but most commonly is similar to CSF with T1 hypointensity and T2 hyperintensity. T2 signal may be hyperintense relative to CSF. These lesions do not enhance with contrast.10,21

Intracranial Lipoma Intracranial lipomas are rare (<0.1%) malformations secondary to faulty differentiation of the primitive meninges.22 They are mostly found in the midline, especially over the corpus callosum in the pericallosal cistern but also in the quadrigeminal and interpeduncular cisterns.23 There is an association with agenesis of the corpus callosum, spinal dysraphism, and other developmental abnormalities of the CNS.24 These lesions are usually incidental findings on imaging studies and very rarely require a surgical intervention. However, they may cause hydrocephalus due to obstruction requiring shunting. Seizures have been reported to be associated with sylvian cistern lipomas.24 On CT, lipomas are well-defined hypodense lesions with occasional peripheral calcification, They usually have a CT density of between −50 Hounsfield units (HU) and −100 HU.23 On MRI, they appear as homogeneous,

hyperintense masses on T1W images (hypointense on fat-suppressed sequences) and hyperintense on T2W images. They do not enhance.23

Epithelial Cysts of the Central Nervous System These lesions are characterized by a glial wall with an epithelial lining similar to ependyma or choroid plexus.25 They are thought to arise from neuroectodermal progenitor cells. Other terms have been used to describe lesions, like ependymal cyst, choroid cyst, choroidal–epithelial cyst, and glioependymal cyst.26 Unless they are very large and cause mass effect, they are asymptomatic and usually found incidentally. On CT, neuroepithelial cysts appear as smooth, round to ovoid, nonenhancing lesions with a central low density resembling CSF. They may display internal septations; they rarely calcify. Intraparenchymal cysts appear well circumscribed with welldefined cyst margins. Because the cyst wall is typically thin, intraventricular cysts and cysts located within the cisterns may be difficult to distinguish from the surrounding CSF. On MRI, the cyst fluid largely resembles CSF on both T1W and T2W images.25 However, the cyst fluid may appear slightly hyperintense to CSF on T1W images. These lesions do not enhance.25,27

Colloid Cysts Colloid cysts account for 0.5–1% of all brain masses. They are commonly third ventricular lesions located anteriorly within the ventricle. Patients present with

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53.  NONNEOPLASTIC MASS LESIONS

headaches, which are secondary to persistent or intermittent obstruction of the foramen of Monro.28 Obstruction resulting in acute hydrocephalus has been described as a cause of sudden death.29 The cell of origin is still a subject of debate but studies suggest an endodermal origin.28,30 Treatment options include observation for small and asymptomatic lesions or surgical management with microsurgical or neuroendoscopic resection.28 Anterior third ventricular location is key in imaging diagnosis of these lesions. CT and MRI signal characteristics are dependent on the composition of the cyst content. T1W signal correlates with cholesterol concentration (two-thirds of them being hyperintense on nonenhanced T1W images), whereas T2W signal is variable. They show no enhancement, not even in the cyst wall.31

Rathke Cleft Cysts Rathke cleft cysts (RCCs) originate from embryonic remnants of Rathke’s pouch and are benign cystic lesions with variable size.32 Content is usually a thick, mucoid material consisting of cholesterol and protein.33 RCCs typically present within the sella in the pars intermedia of the pituitary gland or, rarely, suprasellar.34,35 Small cysts are asymptomatic, incidentally found on imaging. Larger lesions present with signs of mass effect such as headache, pituitary malfunction, or visual field deficits.35 Small, asymptomatic RCCs do not require surgical intervention. When symptomatic, the goal of surgery is cyst drainage and safe removal of as much of the capsule as possible. Cyst fenestration and drainage via an e­ ndonasal/sublabial transsphenoidal approach are the most commonly used methods to achieve this goal.35,36 On imaging, RCCs are well-circumscribed lesions. The pituitary gland is usually around or under the cyst, creating the sign of “the egg in a cup.”37 On CT, they usually appear as low or isodense homogeneous lesions or with & D

slight hyperdensity relative to the brain parenchyma sometimes with ring-like enhancement.36 On MRI, they appear as well-demarcated cystic lesions with homogeneous signal intensity. Signal intensity varies with the composition of the cyst content. T2 hypointense signal intensity is highly suggestive of RCC, as it distinguishes it from chordomas, chondroid tumors, abscesses, mucoceles, and lipomas, all characterized by hyperintense T2 signal.38

Cholesteatoma These are rare middle-ear and mastoid process lesions characterized by destructive, expansile growth. Pathologically, they consist of keratinized squamous epithelium. Patients typically come to medical attention in their 20 s. Most patients present with ear discharge and conductive hearing loss. Less common manifestations are ipsilateral Bell palsy, tinnitus, imbalance, and headaches. Cholesteatomas may be congenital or acquired. The standard management is surgical resection. CT scans through the temporal bones demonstrate a hypodense expansile lesion without enhancement (Figure 1C).39 MRI reveals hyperintense T1W and hypointense T2W signal without postcontrast enhancement. Restricted water diffusion on diffusion-weighted imaging (DWI) helps in distinguishing a cholesteatoma from other middle ear masses.40

Hamartomas CNS hamartomas are slow-growing lesions occurring in the tuber cinereum and inferior hypothalamus. They may be entirely asymptomatic or present with epilepsy (gelastic seizures), developmental delay, and central precocious puberty. They are isointense to normal cortex on T1WI and may be slightly hyperintense on T2WI. Ictal singlephoton emission computed tomography (SPECT) studies have revealed increased perfusion. These lesions do not enhance. Symptomatic lesions may be resected.41,42

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FIGURE 1C  Developmental mass lesions. (a, b) Cholesteatoma (arrowhead). A small mass lesion is noted in the right epitympanum. ((a) High-resolution CT of the right temporal bone, coronal view. (b) T1W with gadolinium). (c) Hamartoma (arrowhead). A hyperintense mass lesion is noted in the left hypothalamus (FLAIR).

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Inflammatory Disorders

INFLAMMATORY DISORDERS Autoimmune Encephalitis These pathologies arise from altered immune response targeting intracellular or cell surface antigens. Limbic encephalitis and rhombencephalitis are often paraneoplastic conditions that typically present in a subacute timeline. The clinical picture may involve confusion, agitation, hallucinations, seizures, and sleep disturbance. Antibodies to onconeural intracellular antigens such as Hu, Ma, and Ri are associated with certain malignancies such as small-cell lung cancer, testicular germcell tumors, thymoma, and Hodgkin lymphoma.43–45 Immune-mediated encephalitis with autoantibodies targeting neuronal cell surface antigens are much more common than those mediated by intracellular antigens, have a better overall prognosis, and are less commonly paraneoplastic.44,45 Treatment includes steroids and immunomodulatory therapy.44,45 T2W and FLAIR sequences reveal hyperintense signal in the medial temporal lobes and hippocampi. This is often subtle and may be entirely absent. When prominent and asymmetric, it may mimic infiltrative or noninfiltrative glioma (pleomorphic xanthoastrocytoma, ganglioglioma).

Primary Central Nervous System Vasculitis Often a multifocal disease affecting small- to mediumsized cerebral blood vessels, primary CNS vasculitis can occasionally present as a mass lesion. Corticosteroids should be used with caution before a definitive diagnosis is established, as they may alter the histopathologic features profoundly. A biopsy is often required. On brain MRI, lesions are hyperintense on T2W images and hypointense on T1W images. There may be patchy contrast enhancement, signs of acute or subacute ischemia, or hemorrhage.46

Sarcoidosis Sarcoidosis is a chronic, multisystem granulomatous inflammatory disease of unclear etiology. A biopsy is required for diagnosis but can often be acquired from extraneural sites. Corticosteroids remain the mainstay of therapy. Sarcoidosis gives rise to a basal meningitis resulting in cranial neuropathies. However, when small parenchymal granulomas coalesce into a single mass it may mimic a neoplastic lesion.47 Large sarcoid granulomas are hypodense on CT. Depending on lesion location they may give rise to obstructive or communicating hydrocephalus. On MRI, lesions on T1W are iso- to hypointense and display variable T2W signal patterns. They enhance after gadolinium administration, as do

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the thickened basal meninges.48,49 Dural involvement may be diffuse or focal and mass-like, and the latter may resemble a meningioma or nerve sheath tumor.6

Inflammatory Pseudotumor Inflammatory pseudotumor (IPT) comprises a heterogeneous group of lesions sharing common histological features (Figure 2). These include fibroblastic and myofibroblastic proliferation with inflammatory infiltrates comprising acute and chronic inflammatory cells, including plasma cells. Infections, malignancies, radiotherapy, and surgery have been reported to precede this pathology.50 IPT has aggressive clinical features and is typically characterized by locally destructive or infiltrative features that mimic malignant neoplasms.76 The usual treatment for brain IPT is surgical resection combined with corticosteroids or radiation therapy. Recurrence is common within 2 years of primary surgery.51 Complete resection is advocated whenever possible.76 CT scans demonstrate lesion enhancement as well as associated bony destruction. On MRI, lesions are T2W hyperintense and enhance homogeneously.52

Rosai–Dorfman Disease Rosai–Dorfman disease (RDD), also referred to as sinus histiocytosis with massive lymphadenopathy, is an uncommon benign lymphoproliferative disorder with an estimated incidence of approximately 100 cases per year in the United States.53,54 It involves the CNS infrequently, usually as dural-based masses. Intraparenchymal involvement is less common.54 In localized presentations, surgical resection is the therapy of choice; however, resection is not always possible and other therapeutic modalities may be required for disease management.54 On CT, RDD lesions present as homogeneous hyperdense masses. Perilesional edema and mass effect on adjacent structures are common. MRI reveals single or multiple well-defined lesions that are isointense on T1W and enhance avidly after gadolinium administration. On T2W RDD lesions appear as heterogeneous masses hypo- or isointense to the contiguous dura.54,55 They have to be distinguished from meningiomas.

Idiopathic Pachymeningitis Idiopathic hypertrophic pachymeningitis is a rare chronic inflammatory process that gives rise to thickening of the dura mater. Mass-like presentations have been described (tumefactive pachymeningitis).56 Histopathologically, there is fibrosis with inflammatory cell infiltration. Patients typically present with cranial neuropathies and headaches, but depending on location and

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(A)

(B)

(C)

(D)

(E)

FIGURE 2  Inflammatory mass lesions. (A) Primary CNS angiitis on the background of congophilic angiopathy. A hyperintense lesion, mostly vasogenic edema, is seen in the right temporoparietal area (T2W). (B) IPT. There is a homogeneously enhancing mass lesion in the thoracic epidural space compressing the cord circumferentially (T1W with gadolinium). (C) Acute demyelinating encephalitis. Two inflammatory lesions surrounded by extensive vasogenic edema are seen in the genu of the corpus callosum and the subependymal white matter in the left centrum semiovale (FLAIR). (D) Single acute demyelinating lesion in the left frontoparietal white matter. There is restriction of water diffusion at the margin. The C-shaped enhancement pattern helps distinguish it from abscesses and rim-enhancing neoplasms (apparent diffusion coefficient map (left), T1W with gadolinium (right)). (E) Paraneoplastic encephalitis. A hyperintense lesion is seen in the left basal ganglia, mesial temporal lobe, and anterior commissure mimicking an infiltrative neoplasm (FLAIR).

extent, a variety of symptoms and signs are possible. Immunosuppression and immunomodulation have been shown to be effective therapies in most patients. On MRI, diffuse, prominent pachymeningeal thickening and enhancement are noted, resembling meningioma en plaque.57 The thickened dura is T1W hypointense and displays mixed signal intensity on T2W.58

Thickening of the cavernous sinus on the afflicted side may be visible on CT. The inflamed dura is iso- to hyperintense on T1W and hyperintense on T2W. Contrast enhancement is common during active disease60 and resolves with steroid therapy.61 As lesions are deep seated and small, patients are often treated empirically, mandating close surveillance imaging.61

Tolosa–Hunt Syndrome

Infundibulitis and Hypophysitis

Tolosa–Hunt syndrome is a steroid-responsive granulomatous disease of the cavernous sinus and orbital apex. Clinical presentation is painful ophthalmoplegia.59

Infundibulitis and hypophysitis are rare clinical entities, which may present alone or in a combined fashion. They are marked by lymphocytic infiltration on

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Infections

histological analysis. Patients may present with diabetes insipidus or other neurohypophyseal endocrinopathies, often in the postpartum period or in the third trimester of pregnancy.62 On MRI the characteristic T2W hyperintense signal of the neurohypophysis is absent. The affected areas are isointense on T1W, hypointense on T2W, and enhance with gadolinium. Pituitary stalk or gland may be thickened, resembling an adenoma.63 Response to steroids or other immunomodulatory agents is highly suggestive of primary autoimmune or lymphocytic etiology.64

Demyelinating Encephalitis Demyelinating disorders may present as cerebral mass lesions. Tumefactive demyelination occurs in the setting of multiple sclerosis and acute disseminated encephalomyelitis. Histopathologically lesions are characterized by demyelination and relative preservation of axon cylinders. Tumefactive lesions of MS are typically periventricular and multiple and follow the course of intramedullary veins. There is little perilesional vasogenic edema or mass effect.65 The lesions are hypointense on T1W and hyperintense on T2W. Enhancement pattern is heterogeneous and creates an incomplete faint ring, an appearance distinguishing demyelination from tumor or abscess.1,66,67 Perfusion-weighted MRI reveals decreased cerebral blood volume in demyelinating tumefactive lesions compared to neoplasms.68 On diffusion-weighted MRI, demyelinating lesions are largely characterized by increased diffusivity in the center of the lesion. Only in the acute stage there may be restricted diffusion in the margin of the lesion.8

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with headaches, nausea, fever, and an altered sensorium. Small abscesses may be eradicated by antibiotherapy alone but most lesions require surgical drainage. Substantial mass effect, periventricular location, signs of increased intracranial pressure, and presence of a foreign body mandate surgical intervention.73 MRI is more sensitive than CT, especially at the early cerebritis stage (Figure 3A). The center of a mature brain abscess is hypointense on T1W and hyperintense on T2W. The surrounding capsule is T2 hypointense and displays peripheral enhancement after contrast administration. Perilesional edema is often profound, a distinguishing feature from tumors.74 Bacterial abscesses in the immunocompetent host are characterized by profound restriction of water diffusion, a feature otherwise seen only in mucoid metastases or epidermoid cysts.71 Occasionally, multiple abscesses may mimic metastatic brain tumors.1 CNS listeriosis affects the brain stem and can mimic an infiltrative glioma. Abscess formation is common.75,76 Tuberculosis can give rise to pachymeningitis, leptomeningitis, and cerebral parenchymal granuloma formation. The last, characterized by central caseous necrosis surrounded by granulomatous inflammation, has to be distinguished from malignant gliomas or metastases. The margin of these lesions enhances avidly. Signal on diffusion-weighted MRI is variable.76 Cerebral syphilitic gumma is a rare manifestation of tertiary syphilis, which is caused by Treponema pallidum. Histopathologically, gummas are granulomatous inflammatory lesions with distinct microvascular changes such as intimal thickening and perivascular inflammation. On MRI, these lesions enhance and are surrounded by vasogenic edema.78

Fungal Infections

INFECTIONS Bacterial Infections and Brain Abscess Brain abscesses are focal, encapsulated infectious lesions within the brain parenchyma. They result from hematogenous or contiguous spread of an infection, penetrating trauma, or barrier breakdown from a neurosurgical procedure. Abscesses from hematogenous spread of bacteria tend to form in the distribution of the middle cerebral artery at the gray–white matter junction.69 Contiguous spread occurs in patients with infections of the paranasal sinuses, middle ear, or mastoid process.70 The most common causative organisms are Streptococcus viridans and Staphylococcus aureus.71 Patients with right to left shunts (arteriovenous fistulas, cardiac defects) are at higher risk. In the immunocompromised host, Nocardia or Listeria species are encountered.72 A detailed exposure history and consideration of endemic pathogens are crucial to establish a definitive diagnosis. Patients present

Fungal brain abscesses resemble bacterial ones. Given their typical occurrence in immunocompromised hosts, appearance on DWI and degree of perilesional vasogenic edema are variable. Examples are cryptococcoma and aspergilloma (Figure 3B). Owing to its tendency to invade blood vessels, aspergillosis may give rise to ischemic strokes.

Parasitic Infections Neurocysticercosis This infection is caused by Taenia solium, whose intermediate host is the pig. Parasitic cysts form at the gray– white matter junction and in the central nuclei. In their final stage, cyst contents are T1W hypointense and T2W hyperintense. Water diffusivity is not restricted. Peripheral enhancement and perilesional vasogenic edema are common.76

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(A)

(a)

(b)

(c)

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FIGURE 3A  Infections. (a) Multiple bacterial abscesses are seen scattered throughout the right internal carotid artery territory, the result of embolization from an infected pseudoaneurysm within the cavernous portion of the vessel (apparent diffusion coefficient map). (b) L ­ isteria rhombencephalitis. Heterogeneous contrast enhancement is noted in brain stem and midline cerebellar structures (T1W with gadolinium). (c) Tuberculosis. Multiple heterogeneously enhancing mass lesions involving dura and cerebral parenchyma are seen in both hemispheres (T1W with gadolinium). (d) Nocardiosis. An abscess is seen in the right parietal region (DWI).

(B) (a)

(b)

(c)

FIGURE 3B  (a) Cryptococcoma of the conus medullaris (arrowhead; T1W with gadolinium). (b) Aspergilloma (diffusion-weighted MRI). (c) Mucor abscess in the right frontal lobe (T1W with gadolinium).

Toxoplasmosis This infection is caused by Toxoplasma gondii, whose definitive host is the cat (Figure 3C). Toxoplasmic lesions have a necrotic center surrounded by inflammatory cells. They occur as single or multiple lesions of variable size and are located at the gray–white matter junction. T1W and T2W images reveal isointense lesions with an irregular and thick rim of enhancement and perilesional vasogenic edema.76

Viral Infections Herpes Encephalitis Herpes simplex encephalitis is the main cause of sporadic viral encephalitis. Like most other pathogenic

viruses, it affects gray matter. Owing to its predilection for the mesial temporal lobe and its asymmetric distribution it can resemble infiltrative glioma. Patients present with altered sensorium and seizures.77 The infection often starts in the anterior part of the temporal lobe and then extends posteriorly. The lesion is T1W hypointense in the acute stage. In the chronic lesion, laminar necrosis is seen as a fine line of T1W hyperintense signal within the cortex. On T2W, areas of inflammation and vasogenic edema are hyperintense. Enhancement is subtle and often peripheral. Gradient-echo sequences may reveal intralesional microhemorrhages. The early lesion is characterized by restricted water diffusion within the cortex reflecting cytotoxic edema. As the disease progresses and neuronal cell membranes are compromised, the apparent diffusion coefficient increases.76

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Other Entities

(C) (a)

(b)

(c)

FIGURE 3C  (a) Toxoplasmosis abscess in the cervical spinal cord (T1W with gadolinium). (b) Herpes simplex encephalitis. Hyperintense s­ ignal is noted, affecting predominantly gray matter of the right temporal lobe (FLAIR). (c) Progressive multifocal leukoencephalopathy. The large lesion affecting both hemispheres displays restriction of water diffusion at its growing edge and increased diffusivity in the center (DWI).

Progressive Multifocal Leukoencephalopathy Progressive multifocal leukoencephalopathy lesions predominantly affect the parieto-occipital white matter. The center of the lesion is T1W hypointense and T2W hyperintense. As cell membrane destruction is complete in this part of the lesion, water diffusivity is increased. Cytotoxic edema and preserved oligodendroglial membranes characterize the margin of the lesion histopathologically. This is reflected by restricted water diffusion.

CEREBROVASCULAR LESIONS Ischemic Infarctions Ischemic strokes, especially at the subacute stage, may occasionally be mistaken for a neoplasm. Wedgeshaped configuration with the broad base on the cortex, involvement of gray and white matter of a single vascular territory (venous or arterial), laminar necrosis, and pseudonormalization on apparent diffusion coefficient support the diagnosis of a stroke. Conversely, early stages of malignant gliomas (markedly increased cellularity without central necrosis) may resemble an ischemic stroke (Figure 4).1

as the initial imaging modality to diagnose acute ICH. Hyperdense in the acute stage, ICH becomes isodense in the subacute stage with possible ring enhancement and hypodense in the chronic stage. On MRI, hyperacute blood is iso- to hypointense on T2W images. In the subacute stage, signal becomes T1W and T2W hyperintense. As macrophages invade the hematoma from the periphery toward the center, T2 signal turns hypointense and T1W signal isointense. Susceptibility weighted imaging (SWI) signal is hyperintense in the acute stage and hypointense in the chronic stage.79 Cavernomas are characterized by heterogeneous central T2W signal and a hypointense rim.80 They are not visible by conventional angiography. Arteriovenous malformation (AVM) has prominent flow voids on T1W and T2W images. SWI sequences may reveal a hypointense rim secondary to previous hemorrhage.81 Differential diagnosis is difficult at the acute stage of acute hemorrhage, such that repeat imaging is often necessary within 6 weeks to identify underlying pathology. Aneurysm are easily diagnosed with CT, MR, and conventional angiography. However, on MRI aneurysms may occasionally resemble a neoplasm, especially when their lumen is partially thrombosed.82

OTHER ENTITIES

Intracranial Hemorrhage Intracranial hemorrhage (ICH) may have a mass-like appearance. It results from uncontrolled hypertension, trauma, or vascular lesions such as hemorrhagic stroke, arteriovenous malformation, aneurysm, or dural sinus thrombosis. An important feature of intracranial hemorrhage imaging is the evolution over time secondary to degradation of blood products. Treatment is defined by the causative pathology, but if the hemorrhage is large enough to cause mass effect or hydrocephalus, surgical intervention may be required. Head CT is widely used

Extramedullary Hematopoiesis Mostly related to thalassemia and myelofibrosis, extramedullary hematopoiesis is rare in the cranial vault and the spinal canal and is usually an incidental finding, but on rare occasions it can cause mass effect and present with neurologic dysfunction. CT reveals heterogeneous density in the extra-axial space (Figure 5). MRI demonstrates extra-axial masses that are isointense on T1W and hypointense on T2W images with postcontrast enhancement.83,84

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(A)

(B)

(C)

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(D)

FIGURE 4  Cerebrovascular lesions mimicking tumors and vice versa. (A–C) Subacute ischemic infarction in the right anterior cerebral artery territory. There is susceptibility artifact in a cortical pattern indicative of hemorrhagic transformation ((A) DWI; (B) susceptibility-weighted MRI; (C) FLAIR). (D) A small area of restricted water diffusion indicative of increased cellularity is noticed in the right frontal parasagittal region. Biopsy revealed glioblastoma multiforme. (E) A left frontal hematoma is seen in the left frontal lobe. Repeat imaging 2 months later shows a heterogeneously enhancing mass lesion within the resolving hematoma. Biopsy revealed malignant glioma.

(A)

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FIGURE 5  Other entities. (A) Extramedullary hematopoiesis. A hyperintense mass lesion compresses the thoracic spinal cord posteriorly (arrowheads; T1W). (B) Amyloidoma. A subependymal heterogeneously enhancing mass lesion is seen adjacent to the body of the left lateral ventricle. Biopsy revealed amorphous material identified as β-amyloid by immunohistochemistry (T1W with gadolinium). (C) Radiation necrosis. A superficial inflammatory mass is seen in the right parietal lesion (arrowheads). There is extensive vasogenic edema in the underlying white matter. The patient had received radiosurgery to a scalp melanoma (T2W). (D) Polymorphic posttransplant lymphoproliferative disorder. A heterogeneously enhancing mass lesion is seen in the left frontal parasagittal region (T1W with gadolinium).

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References

Amyloidoma Like in amyloid angiopathy and senile plaques, amyloidoma is also formed by the deposition of amyloid protein and presents as single or multiple intracranial masses. Surgical intervention may be required for diagnosis but only rarely for mass effect. Imaging characteristics including enhancement patterns vary.85

Radiation Necrosis Radiation necrosis (RN), also referred to as pesudoprogression, poses a considerable diagnostic challenge as it is difficult to differentiate from tumor recurrence. Clinically, both pathologies present with signs and symptoms of focal mass effect. Therapy involves corticosteroids, bevacizumab, or surgical intervention. Radiologically, a “soap bubble” appearance on post-gadolinium sequences has been described as characteristic for RN. Perfusionweighted MRI may reveal increased cerebral blood volume in tumors and decreased cerebral blood volume in RN. [18F]Fluorodeoxyglucose PET, SPECT, and MR spectroscopy provide additional information but none of these studies has sufficient sensitivity or specificity.86

Polymorphic Posttransplant Lymphoproliferative Disorder Occurring in organ transplant recipients on chronic immunosuppression, these lesions represent unchecked B-cell polyclonal or oligoclonal hyperplasia and may involve the CNS. Clinical symptoms are variable and depend on the location of the lesions. First-line therapy is reduction of immunosuppression. They may present as multiple hemispheric masses with variable MRI features and enhancement patterns, depending on their cellularity. Left untreated, degeneration into lymphoma occurs. This is reflected by MRI findings (restriction of water diffusion, homogeneous or rim enhancement.87

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