Opening Round

Neuroradiology: THE REQUISITES, 2nd ed, pp 148–152.

Comment

Metastatic disease is among the most common causes of intracranial masses in adults. Metastases are frequently multiple; however, in 30% to 50% of cases, they may occur as an isolated lesion on imaging. Enhanced MR imaging is clearly more sensitive than CT in detecting cerebral metastases. Metastases are typically circumscribed masses that demonstrate variable enhancement patterns (solid, peripheral, or heterogeneous). Metastases are often associated with a disproportionate amount of surrounding edema, manifested on T2-weighted (T2W) images as increased signal intensity in the adjacent white matter.

Metastases typically occur at the gray–white matter interface because tumor cells lodge in the small-caliber vessels in this location. Metastatic deposits may also involve the cortex. With cortical metastases in particular, edema may be absent such that metastatic lesions could be missed on T2W imaging. Therefore, it is essential to give intravenous contrast to patients with suspected brain metastases. Studies examining the role of double- and triple-dose gadolinium have shown that although higher doses of contrast reveal more lesions than does a single dose, this often occurs in patients whose standard-dose study already shows more than one metastasis. Therefore, management in these patients is not affected, and multidose gadolinium is neither indicated nor recommended. In patients with no or a single metastasis on single-dose gadolinium, higher doses of contrast material yield additional metastases in fewer than 10% of cases.

Hypointensity (T2W shortening) may be seen with blood products, as a result of the paramagnetic effects of melanin, and when lesions have calcification, hypercellularity, or proteinaceous material. In both cases seen here the patients have hemorrhagic metastatic melanoma. Case A has multiple small metastases at the gray–white junction, and Case B has a solitary large hemorrhagic metastasis with a fluid-hemorrhage level. Even though vascular tumors, such as renal and thyroid carcinoma, and melanoma have a propensity to bleed, because breast and lung carcinoma are much more common, a hemorrhagic metastasis is more likely to be related to one of these cancers. In the case of a single cerebral hemorrhagic mass, primary brain tumors, such as glioblastoma multiforme, should be considered.

Notes

CASE 4 Penetrating Brain Injury—Bow and Arrow Injury

1. What are the imaging findings?

2. What would Quincy, MD, say about how this injury occurred?

3. What is the most effective, efficient way to work up a penetrating head injury?

4. What are the potential causes of the intracranial air?

1. There is a penetrating injury to the head, with frontal lobe hemorrhage and intraventricular extension, and there is a retained bow and arrow.

CASE 4

2. I may be dating myself (Quincy, MD, was a famous TV forensic pathologist), but he would say that this was a self-inflicted injury. The trajectory was entrance under the mandible (submental) and then through the anterior cranial fossa.

3. Computed tomography: short and sweet!

4. Intracranial air may be due to a communication with the extracranial compartment (open fracture) or may indicate an associated fracture through an adjacent paranasal sinus or the temporal bone.

Kriet et al. 2005 Kriet JD, Stanley RB, Grady MS. Self-inflicted submental and transoral gunshot wounds that produce nonfatal brain injuries: management and prognosis. J Neurosurg. 2005;102:1029-1032.

Neuroradiology: THE REQUISITES, 2nd ed, pp 255–256.

Comment

Penetrating injuries cause lacerations of the brain and its coverings (dura), and these are associated with gunshot wounds, stab wounds (in this case, a self-inflicted bow and arrow injury), or displaced bone fragments. With penetrating wounds, there is a risk of injury to critical structures that are in the trajectory of the penetrating object. Brain injury may result in functional and cognitive losses, depending on the region of the brain injured. Injury to the intracranial arteries may result in dissection, occlusion, hemorrhage, or pseudoaneurysm formation. Pseudoaneurysms must always be considered because they have a very high incidence of delayed hemorrhage. Occasionally, arteriovenous fistulas may occur intracranially, although these are more common with penetrating injuries to the neck. Computed tomography is the most efficient and effective way to assess a penetrating brain injury rapidly. It can determine whether a surgical emergency is present, such as an acute hemorrhage with mass effect necessitating acute surgical decompression. It also shows the location and extent of retained foreign bodies. Computed tomography also identifies intracranial air that is due to communication with the extracranial compartment (open fracture) or may indicate an associated fracture through an adjacent paranasal sinus or the temporal bone. Trapped intracranial air may result in tension pneumocephalus related to a one-way ball valve mechanism that causes gradual expansion of the intracranial air and mass effect on the adjacent brain.

Notes

CASE 5 Orbital Pseudotumor

Jacobs D, Galetta S. Diagnosis and management of orbital pseudotumor. Curr Opin Ophthalmol. 2002;13:347-351.

Neuroradiology: THE REQUISITES, 2nd ed, pp 504–505.

Comment

Orbital pseudotumor, also known as idiopathic orbital inflammatory syndrome, is a nonspecific inflammation of unknown etiology that involves the contents of the orbit. Clinical presentations include proptosis, pain, and decreased ocular motility. This disorder is usually unilateral, but may be bilateral in fewer than 10% of patients. Orbital pseudotumor should be considered a diagnosis of exclusion, with evaluation directed at eliminating other causes of orbital disease. Underlying systemic disorders should be considered, including sarcoid, lymphoma, connective tissue disease, Wegener’s granulomatosis, and autoimmune disorders. In the early stages of orbital pseudotumor, histologic features are characterized by inflammation and edema, with an abundance of lymphocytes, plasma cells, and giant cells. In the late stages of disease, fibrosis may be abundant. Orbital pseudotumor may present with a spectrum of manifestations, including myositis (as in this case), dacryoadenitis (lacrimal gland involvement), periscleritis (uveal and scleral thickening), or retrobulbar soft tissue abnormality. In myositis, pseudotumor may involve one or more muscles, and unlike thyroid ophthalmopathy, it often involves the tendinous insertion of the muscle as well as the muscle bellies. When idiopathic inflammation primarily involves the cavernous sinus and the orbital apex, it is referred to as Tolosa-Hunt syndrome. Ophthalmoplegia is secondary to involvement of cranial nerves III through VI in the cavernous sinus.

Because orbital pseudotumor radiologically may appear similar to a variety of disease processes, patient history is important (pseudotumor is classically associated with pain and acute onset). Importantly, there is usually a dramatic response to steroids that may be useful in confirming the diagnosis of pseudotumor. A small percentage of patients do not respond to steroids and may require radiation or chemotherapy.

Notes

CASE 6 Acute Epidural Hematoma and Associated Linear Fracture of the Frontal Bone

Hamilton M, Wallace C. Nonoperative management of acute epidural hematoma diagnosed by CT: the neuroradiologist’s role. AJNR Am J Neuroradiol. 1993;13:853-859.

Neuroradiology: THE REQUISITES, 2nd ed, pp 247–248.

Comment

There are two anatomic types of extra-axial collections or hematomas, namely, subdural and epidural. On CT imaging acute epidural hematomas are hyperdense extra-axial masses that can usually be distinguished from acute subdural hematomas based on their shape and location relative to the calvarial sutures. Epidural hematomas are usually confined by the cranial sutures because the dura is adherent to the periostium of the inner calvarium. This results in the biconvex or lenticular shape of these collections, which occur between the dura and the periostium. In comparison, subdural hematomas cross sutural boundaries because they occur deep to the dura, occupying the space between the dura and pia arachnoid along the surface of the brain. As a result, subdural collections or hematomas tend to be crescentic in shape, similar to a sliver of the moon.

In the vast majority of cases (80%–90%), epidural hematomas are secondary to a direct laceration of the meningeal arteries (most commonly the middle meningeal artery) by an overlying skull fracture. In a small percentage of cases (<20%), epidural hematomas occur due to tearing of meningeal arteries in the absence of a fracture. This is most commonly seen in children and may be related to transient depression of the incompletely ossified soft calvarium, resulting in laceration of a meningeal artery. Most arterial epidural hematomas occur in the temporal region, although they may be seen in the frontal or temporoparietal regions.

Epidural hematomas due to venous rather than arterial injury are much less common. Venous epidural hematomas are usually due to tearing of a dural venous sinus related to an underlying calvarial fracture. They are most common in the posterior fossa as a result of injury to the transverse or sigmoid sinuses, and are most frequently seen in the pediatric population. Unlike arterial epidural hematomas and subdural hematomas, venous epidural hematomas may extend across the tentorium cerebelli and involve both the supratentorial and infratentorial compartments. These may also occur in a paramedian location over the cerebral convexities or in the middle cranial fossa as the result of a tear in the superior sagittal or sphenoparietal sinus, respectively.

Other traumatic sequelae that may occasionally be seen in the setting of epidural hematomas include pseudoaneurysms of the meningeal artery (most commonly the middle meningeal artery) and arteriovenous fistulas if a fracture lacerates both the middle meningeal artery and vein, resulting in their communication.

Notes

CASE 7 Pyogenic Brain Abscess

Nowak DA, Rodiek SO, Topka H. Pyogenic brain abscess following haematogenous seeding of a thalamic haemorrhage. Neuroradiology. 2003;45:157-159.

Tung GA, Rogg JM. Diffusion-weighted imaging of cerebritis. AJNR Am J Neuroradiol. 2003;24:1110-1113.

Neuroradiology: THE REQUISITES, 2nd ed, pp 282–284.

Comment

The development of a pyogenic brain abscess may be divided into four stages: early cerebritis (1–3 days), late cerebritis (4–9 days), early capsule formation (10–13 days), and late capsule formation (14 days and after). The length of time required to form a mature abscess varies from approximately 2 weeks to months. In the mature abscess there is a collagen capsule that is slightly thinner on the ventricular side than on the cortical margin (this may be related to differences in perfusion). The presence of a dimple or small evagination pointing toward the ventricular margin from a ring-enhancing lesion should raise suspicion for an abscess. This is also important because intraventricular rupture and ependymitis may occur and are associated with a very poor prognosis. In the presence of a mature abscess, there is relatively little surrounding cerebritis and edema compared with the early stages of abscess formation. A circumferential rim that is isointense to slightly hyperintense to white matter on unenhanced T1-weighted (T1W) images and hypointense on T2-weighted (T2W) images may be present around a brain abscess. This appearance may be related to the presence of collagen, free radicals within macrophages, or small areas of hemorrhage. Diffusion-weighted imaging may be very helpful because the high signal intensity of the pus-filled necrotic center may show restricted diffusion (low apparent diffusion coefficient), differentiating an abscess from a necrotic neoplasm, as in this case.

The management of a mature brain abscess is surgical drainage and antibiotic therapy. Cerebritis and early abscesses may be managed with antibiotics and should be followed closely both with MR imaging and clinically for signs of improvement or deterioration. Successful management monitored with serial MR imaging examinations will show a decrease in the surrounding edema, mass effect, and associated enhancement. It is important to remember that radiologic findings lag behind clinical improvement, and enhancement may persist for months. Resolution of an abscess may result in an area of gliosis with small calcifications.

Notes

CASE 8 Chiari II Malformation with Associated Anomalies

1. What is the in utero abnormality that results in these malformations?

2. What cervical spine anomalies are frequently associated with these malformations?

3. Which type of Chiari malformation is associated with a myelomeningocele?

4. What are the accepted normal limits in children and adults for the inferior position of the cerebellar tonsils relative to the foramen magnum?

1. Dorsal induction–neural tube defects.

CASE 8

2. Klippel-Feil syndrome, partial fusion of C2 and C3, occipitalization of the atlas (partial or complete fusion of C1 with the occiput), and a hypoplastic ring of C1.

3. Chiari II malformation.

4. Cerebellar tonsil position relative to the foramen magnum varies with age. In children younger than 10 years of age, 6 mm or less is considered within normal limits. In adulthood, 3 mm or less is within normal variation. Typically, low-lying tonsils that are within normal variation are rounded in contour.

Naidich TP, McLone DG, Fulling KH. The Chiari II malformation: part IV. The hindbrain deformity. Neuroradiology. 1983;25:179-197.

Royal SA, Tubbs RS, D’Antonio MG, Rauzzino MJ, Oakes WJ. Investigations into the association between cervicomedullary neuroschisis and mirror movements in patients with Klippel-Feil syndrome. AJNR Am J Neuroradiol. 2002;23:724-729.

Neuroradiology: THE REQUISITES, 2nd ed, p 437.

Comment

Chiari malformations typically occur during the first 3 to 4 weeks of gestational life and are dorsal induction–neural tube defects. Chiari II malformations are the most common symptomatic form. This case illustrates all of the findings of Chiari II malformations, which are reviewed later. In Chiari II malformations, the vermis, cerebellar tonsils, and medulla herniate into the foramen magnum and upper cervical canal. The cerebellar hemispheres wrap around the brain stem, the cerebellar vermis herniates up through the tentorial incisura (“towering cerebellum”), and the tectum is “beaked.” The fourth ventricle is elongated and displaced inferiorly. Chiari II malformations are associated with a spectrum of supratentorial anomalies, including dysgenesis of the corpus callosum (most commonly splenial anomalies) and heterotopias or sulcation abnormalities, as illustrated in this case. Myelomeningoceles are seen in virtually all Chiari II malformations, and more than 50% of cases are associated with syringohydromyelia.

In Chiari I malformations, there is herniation of the cerebellar tonsils, which are pointed (peg-like) in configuration into the cervical spinal canal. The remainder of the cerebellum, brain stem, and fourth ventricle are normal in location. Syringohydromyelia is frequently seen in Chiari I malformations; myelomeningoceles are not.

Chiari III malformations have the same findings as Chiari II malformations, but also include herniation of the posterior fossa contents into a high cervical or occipital encephalocele. There is no associated lumbosacral myelomeningocele.

Notes

CASE 9 Acute Hydrocephalus Secondary to Meningitis

Daoud AS, Omari H, Al-Shayyab M, Abuekteish F. Indication and benefits of computed tomography in childhood bacterial meningitis. J Trop Pediatr. 1998;44:167-168.

Gammal TE, Allen MBJr, Brooks BS, Mark EK. MR evaluation of hydrocephalus. AJR Am J Roentgenol. 1987;149:807-813.

Neuroradiology: THE REQUISITES, 2nd ed, pp 374–377.

Comment

Obstructive hydrocephalus can be categorized as communicating or noncommunicating. Noncommunicating hydrocephalus is usually related to obstruction of CSF flow at some level within the ventricular system and is commonly related to neoplasms; however, infection, hemorrhage, cysts, or congenital lesions (synechiae, webs, arachnoid cysts) may be responsible. Communicating hydrocephalus typically results from obstruction of the arachnoid villi, foramen magnum, or tentorial incisura. Common causes of communicating hydrocephalus include inflammation of the meninges, or meningitis (as in this case; the patient has bacterial meningitis); ventriculitis; subarachnoid hemorrhage; and carcinomatous meningitis. Obstruction of the arachnoid villi in these situations is usually related to high protein concentrations, hemorrhage, or hypercellularity of the CSF. In bacterial meningitis, purulent exudate in the subarachnoid spaces over the cerebral convexities and in the basilar cisterns, where CSF flow is more sluggish, results in impairment of CSF absorption by the arachnoid villi.

On imaging, dilation of the anterior third ventricle in particular is most indicative of hydrocephalus and should not be present in normal subjects or in patients with atrophy. Elevation and thinning of the corpus callosum, best appreciated on sagittal MR imaging, is present in more than 75% of cases of hydrocephalus. Acute hydrocephalus may manifest with hypodensity around the ventricles on CT scans or hyperintensity on MR T2W images in the periventricular white matter due to transependymal flow of CSF. Compensated long-standing hydrocephalus usually does not present with this finding. Treatment of noncommunicating and communicating hydrocephalus is different. Noncommunicating hydrocephalus often requires surgery (e.g., resection of a neoplasm), whereas communicating hydrocephalus is usually treated with shunting.

Notes

CASE 10 Pineal Cyst

Barboriak DP, Lee L, Provenzale JM. Serial MR imaging of pineal cysts: implications for natural history and follow-up. Am J Roentgenol. 2001;176:737-743.

Neuroradiology: THE REQUISITES, 2nd ed, pp 161–162.

Comment

The pineal gland develops during the second month of gestation as a diverticulum in the diencephalic roof of the third ventricle. Pineal cysts are common incidental findings on MR imaging of the head obtained for unrelated indications, seen in 1% to 4% of patients. In autopsy series, cystic lesions of the pineal gland have been found in 20% to 40% of specimens. Masses of the pineal gland may cause mass effect on the tectum and the aqueduct, resulting in paralysis of upward gaze (Parinaud’s syndrome) and hydrocephalus or headache, respectively. However, even large pineal cysts rarely are symptomatic. Pineal cysts are variable in size, and 50% of cysts identified on MR imaging are larger than 1 cm. Studies have shown that, overall, the majority of cysts do not change in size; however, small changes in size (increases and decreases) have been noted. Enlargement of these cysts may be due to increased cyst fluid or intracystic hemorrhage. Rare cases of pineal apoplexy have been reported in which there may be sudden death as a result of intracystic hemorrhage and acute hydrocephalus.

Pineal cysts are less common in young children and are usually seen in middle-aged adults, suggesting that these cysts may develop in late childhood or adolescence and later involute. Pineal cysts are homogeneous on MR imaging. They are typically well demarcated and round or oval, and have a thin or imperceptible wall. On proton density–weighted and FLAIR imaging (as in this case), the cyst contents are frequently hyperintense relative to cerebrospinal fluid. Nodular enhancement of the wall should not be present with cysts. Asymptomatic, larger cysts may cause tectal deformity.

Notes

CASE 11 Hemorrhagic Contusion—Closed Head Injury

1. What are the findings and what is the diagnosis?

2. What are characteristic locations of cortical contusions in the setting of acceleration–deceleration injuries?

3. What are potential causes of blood–fluid levels in a traumatized brain?

4. What structures on a head CT normally enhance after intravenous administration of contrast material?

1. There are multiple regions of intraparenchymal high density consistent with hemorrhage, and associated surrounding edema. The pattern of intracranial hemorrhage is consistent with multiple contusions in the setting of closed head injury.

CASE 11

2. The anterior and inferior temporal and frontal lobes, as well as the posterolateral temporal lobes and the occipital poles.

3. Hemorrhage into injured necrotic brain or blood dyscrasias (abnormal coagulation).

4. Structures without a blood–brain barrier (choroid plexus, pituitary stalk, pineal gland, mucous membranes, extraocular muscles), and the blood vessels of the cavernous sinuses. It is important to be able to determine whether images are contrast enhanced because acute hemorrhage has a similar density to iodinated contrast material.

Oertel M, Kelly DF, McArthur D, et al. Progressive hemorrhage after head trauma: predictors and consequences of the evolving injury. J Neurosurg. 2002;96:109-116.

Neuroradiology: THE REQUISITES, 2nd ed, pp 254–255.

Comment

Hemorrhagic contusions are among the most common traumatic brain injuries. Contusions represent petechial hemorrhages in the cortex that may extend into the adjacent white matter and are frequently associated with adjacent subarachnoid blood. They tend to occur along the superficial surfaces of the brain and are the result of acceleration (boxing) and deceleration forces (motor vehicle accident with head impact, such as against the steering wheel or side window) that cause the brain to rub along surfaces where there are prominent osseous ridges or dural reflections. The anterior and inferior portions of the temporal and frontal lobes, the posterolateral temporal lobes, and the occipital poles are typically contused in acceleration–deceleration injuries, as in this case. The surfaces of these portions of the brain rub against the floor and anterior walls of the anterior and middle cranial fossae, sphenoid wings, temporal bones, and petrous ridges. Hemorrhagic contusions may also occur in the setting of penetrating trauma (gun and knife club-type injuries, depressed skull fractures, or iatrogenic causes). Contusions may also occur along the convexities of the cerebral hemispheres adjacent to the midline as a result of the brain rubbing against the rigid falx or the surface of the inner table of the calvaria.

Imaging findings will depend on when the patient is imaged relative to the time of injury. In the acute setting, hemorrhages are hyperdense and are frequently associated with surrounding hypodensity that represents edema. Acute hemorrhagic contusions are hypointense on T2W, FLAIR, and gradient echo MR imaging, with surrounding high signal intensity due to edema. Long-term follow-up shows resolution of the hemorrhage, encephalomalacia in the area of traumatized brain, and hemosiderin in the contusion bed.

Notes

CASE 12 Juvenile Pilocytic Astrocytoma of the Cerebellum

Viano JC, Herrera EJ, Suarez JC. Cerebellar astrocytomas: a 24-year experience. Child Nerv Syst. 2001;17:607-610.

Neuroradiology: THE REQUISITES, 2nd ed, pp 119, 121–123, 132.

Comment

Astrocytomas are the most common intracranial tumors in children, accounting for up to 50% of such neoplasms. Approximately two thirds are located in the posterior fossa. Cerebellar astrocytomas and medulloblastomas are the most common infratentorial neoplasms in children. Approximately 80% of all cerebellar astrocytomas in children are of the pilocytic variety. Most patients with pilocytic astrocytomas have normal karyotypes; however, long arm deletions of chromosome 17 have been associated with them as well. It is important that both radiologists and neuropathologists be able to distinguish pilocytic astrocytomas from the less common but more aggressive anaplastic fibrillary types because prognosis and management are distinctly different. Pilocytic astrocytomas represent one of the more benign forms of glial neoplasms and are classified as circumscribed gliomas by the World Health Organization. Histologically, tightly packed, piloid processes arising from tumor cells are typical, as are microscopic and macroscopic cysts. Eosinophilic granular bodies and Rosenthal fibers (astrocytic processes) are also present. The prognosis is usually excellent after surgical management. Conversely, higher-grade infiltrative astrocytomas have a poor prognosis.

Pilocytic astrocytoma has a characteristic appearance. Typically, these tumors are well-circumscribed masses that usually arise within the cerebellar hemisphere (but may arise in the midline or vermis, as in this case), with a unilocular cyst and an enhancing solid mural nodule. Usually the cystic component follows the signal characteristics of CSF on all MR imaging pulse sequences. The wall of the cyst does not usually enhance; however, rim enhancement of the cyst can occur and may be related to enhancement of normal adjacent cerebellar parenchyma. Calcification and hemorrhage are uncommon in juvenile pilocytic astrocytomas.

Notes

CASE 13 Fibrous Dysplasia

Chong VF, Khoo JB, Fan YF. Fibrous dysplasia involving the base of the skull. AJR Am J Roentgenol. 2002;178:717-720.

Neuroradiology: THE REQUISITES, 2nd ed, pp 513, 662, 864.

Comment

Fibrous dysplasia is a nonhereditary developmental disorder of the bone forming mesenchyma in which osteoblasts do not undergo normal differentiation and maturation. Medullary bone is replaced with fibrous tissue. Trabeculae of woven bone contain fluid-filled cysts embedded in a collagenous fibrous matrix. The etiology is unknown. Fibrous dysplasia may be monostotic (a solitary lesion) or polyostotic (lesions in multiple bones or multiple lesions in one bone). The majority (approximately 75%) of cases are monostotic. Polyostotic fibrous dysplasia more commonly involves the skull and facial bones, pelvis, spine, and shoulder. Polyostotic disease more commonly is unilateral in distribution. Common areas of calvarial involvement include the ethmoid, maxillary, frontal, and sphenoid bones. Involvement of these bones may result in orbital abnormalities such as exophthalmos, visual disturbances, and displacement of the globe. Involvement of the temporal bone may result in hearing loss or vestibular dysfunction. Although Paget’s disease may occur in these same locations of the calvaria, unlike fibrous dysplasia, concomitant involvement of the facial bones is less common.

Cutaneous pigmentation is the most common extraskeletal manifestation in fibrous dysplasia. It occurs in more than 50% of cases of the polyostotic form. Cutaneous pigmentation is ipsilateral to the side of bony lesions, a feature that differentiates this disease from pigmentation in neurofibromatosis. The pigmented macules, or café-au-lait spots, are related to increased amounts of melanin in the basal cells of the epidermis. They tend to be arranged in a linear or segmental pattern near the midline of the body, usually overlying the lower lumbar spine, sacrum, upper back, neck, and shoulders.

This patient has features typical of fibrous dysplasia. There is a “ground glass” appearance of the involved clivus, occipital bones, and left temporal bone. There is relative preservation of the cortex and expansion of involved bones that maintain their normal configuration.

Notes

CASE 14 Acute Middle Cerebral Artery Stroke: “Hyperdense” Middle Cerebral Artery and Insular Ribbon Sign

Lev MH, Farkas J, Gennete JJ, et al. Acute stroke: improved nonenhanced CT detection—benefits of soft-copy interpretation by using variable window width and center level settings. Radiology. 1999;213:150-155.

Neuroradiology: THE REQUISITES, 2nd ed, pp 86–88, 183–187.

Comment

An unenhanced head CT scan is the first imaging study for the emergent evaluation of acute stroke because it is readily available, rapidly performed, and sensitive in identifying acute intracranial hemorrhage. Specific imaging findings in the assessment of acute stroke include focal parenchymal hypoattenuation (in the insular ribbon or basal ganglia for MCA infarcts), cerebral mass effect manifested as sulcal effacement, and the “hyperdense” MCA sign. Initial unenhanced CT scans show hypoattenuation in up to 80% of patients with acute MCA strokes, some degree of brain swelling in one third of cases, and hyperattenuation of the MCA in 10% to 45% of patients. In early strokes, thrombolytic therapy may be used either intravenously or intra-arterially with angiographic guidance. Before interventions with clot busters, detection of acute hemorrhage or infarction is important because these conditions are relative contraindications to such therapy.

Ischemic changes on CT scans may be predictive of outcome, response to thrombolytic therapy, and regions likely to become infarcted. In the European Cooperative Acute Stroke Study there was an increased risk of fatal parenchymal hemorrhage in patients with hypoattenuating areas greater than one third the MCA territory or mass effect. Hence, these findings are considered by some to be contraindications to thrombolytic treatment. The National Institute of Neurological Disorders and Stroke (NINDS) Study showed a benefit from thrombolytic agents administered intravenously within 3 hours of stroke onset, and there was a trend toward improved outcome despite initial CT-observed regions of hypoattenuation. The European Cooperative Acute Stroke Study suggested that the subgroup of patients with acute stroke and without demonstrable ischemia on CT scans is also unlikely to benefit from intravenous thrombolysis.

Magnetic resonance imaging is more sensitive than CT in detecting acute infarcts. MR imaging has also shown extension of infarctions on follow-up examinations. It is identification of this “penumbra” (brain tissue at risk for irreversible ischemia) that is at the heart of further development of CT and MR imaging techniques. It is important to protect this tissue from ischemia by applying appropriate interventions. Furthermore, to deliver protective agents, perfusion to this tissue is necessary.

Notes

CASE 15 Multiple Sclerosis

1. What is Balo’s concentric sclerosis?

2. What is the pathologic hallmark of an acute, active demyelinating plaque?

3. What percentage of patients with multiple sclerosis have isolated spinal cord disease?

4. What is Devic’s disease?

1. Balo’s concentric sclerosis is an uncommon demyelinating disorder characterized on MR imaging and pathologically as lesions with a laminated appearance that reflect alternating regions of demyelinated and myelinated tissue. Concentric or laminated contrast enhancement is noted around the lesion with a core that is more similar to CSF in signal. This may represent a rare demyelinating disorder separate from multiple sclerosis, but such lesions may be seen in patients with multiple sclerosis.

CASE 15

2. Perivenual inflammatory changes.

3. Approximately 8% to 12%. In patients presenting with myelopathy and an MR imaging study that reveals a cord lesion, multiple sclerosis should be considered. Evaluation should include complete spinal cord and brain MR imaging.

4. Involvement of the spinal cord and/or optic pathways (this may be simultaneous or separated in time) without brain involvement on imaging.

Loevner LA, Grossman RI, McGowan JC, Ramer KN, Cohen JA. Characterization of multiple sclerosis plaques with T1-weighted MR and quantitative magnetization transfer. AJNR Am J Neuroradiol. 1995;16:1473-1479.

Rovaris M, Comi G, Ladkani D, Wolinsky JS, Filippi M, European/Canadian Glatiramer Acetate Study Group. short-term correlations between clinical and MR imaging findings in relapsing-remitting multiple sclerosis. AJNR Am J Neuroradiol. 2003;24:75-81.

Neuroradiology: THE REQUISITES, 2nd ed, pp 332–347.

Comment

This case shows numerous white matter lesions with a periventricular predominance. Lesions are also noted in the body of the corpus callosum and the subcortical white matter. The largest lesion in the right frontal white matter has a demarcated central region that follows the signal characteristics of CSF on all pulse sequences, with a peripheral rim, or “halo,” that has restricted diffusion (image 3) and enhancement consistent with active demyelination.

Most acquired diseases involving the white matter have similar MR imaging findings. Patient age, history, and physical examination are of paramount importance in limiting the differential diagnosis, which may include vasculopathies (small vessel ischemic disease, vasculitis, hypertension, migraines), demyelinating disease, and inflammatory processes (Lyme disease, sarcoid).

Multiple sclerosis is a chronic inflammatory disease characterized by relapsing or progressive demyelinating plaques in the brain and spinal cord. Multiple sclerosis affects the oligodendrocytes. In the acute stage, plaques have an inflammatory reaction with edema, cellular infiltration, and a spectrum of demyelination. Plaques tend to be in a perivenous distribution. Chronic lesions show astrocytic hypoplasia, resolution of the cellular infiltration, and loss of myelin. The diagnosis of multiple sclerosis is a clinical one; however, MR imaging may be extremely helpful in supporting the diagnosis. On T1W images, plaques may be isointense to hypointense to the brain. Hypointense lesions are chronic and most likely are associated with gliosis and significant myelin loss. FLAIR imaging is particularly helpful in identifying lesions in the periventricular white matter or along CSF interfaces because suppression of water results in increased lesion conspicuity. Lesions at the callosal–septal interface are highly suggestive of multiple sclerosis. Contrast administration allows separation of lesions with an abnormal blood–brain barrier (enhancing lesions) from those with an intact blood–brain barrier (nonenhancing lesions). A lesion that has restricted diffusion also indicates active demyelination. MR imaging is also more sensitive than clinical examination in detecting active disease in clinically silent areas of the brain.

Notes

CASE 16 Meningioma

Alvernia JE, Sindou MP. Preoperative neuroimaging findings as a predictor of the surgical plane of cleavage: prospective study of 100 consecutive cases of intracranial meningioma. J Neurosurg. 2004;100:422-430.

Sheporaitis LA, Osborn AG, Smirniotopoulos JG, et al. Intracranial meningioma. AJNR Am J Neuroradiol. 1992;13:29-37.

Neuroradiology: THE REQUISITES, 2nd ed, pp 98–105.

Comment

Meningiomas are the most common intracranial, extra-axial neoplasm. Although there are a variety of histologies, including fibroblastic, angioblastic, syncytial, and transitional types, prognosis is not primarily dependent on the histology but rather on the location of the meningioma. Large meningiomas occurring over the cerebral convexities may be treated with embolization when necessary, followed by surgery without neurologic deficit; in contrast, meningiomas as small as 1 cm involving the cavernous sinus may be very symptomatic and present a more challenging treatment dilemma. Meningiomas occur most commonly in middle-aged women; however, they are also found frequently in men. Most meningiomas are sporadic, isolated lesions. Multiple meningiomas may be familial or may be seen in patients with a history of radiation therapy to the brain, neurofibromatosis type 2, and basal cell nevus (Gorlin-Goltz) syndrome.

On unenhanced CT, more than 50% of meningiomas are hyperdense (as in this case). Approximately 20% to 25% are associated with calcification or a reaction in the adjacent bone (hyperostosis is more common than osteolysis). The bone window in this patient shows that the mass is calcified, but close inspection of the inner cortical table shows secondary “blistering.” On MR imaging, meningiomas are often isointense to gray matter on T1W and T2W sequences; however, they may be hyperintense on T2W imaging. Meningiomas typically have avid, homogeneous enhancement. The most important clue to making the diagnosis of a meningioma is in establishing that the mass is extra-axial. One finding consistent with an extra-axial location is the presence of a pseudocapsule, which may represent CSF, dura, or vessels along the pia-arachnoid. Although the presence of an enhancing dural tail is highly suggestive of meningioma, this is a nonspecific finding and may be seen in other disease processes.

Notes

CASE 17 Acute Actively Bleeding Subdural Hematoma—Subfalcine Herniation and Stroke

Gentry LR, Godersky JC, Thompson B, Dunn VD. Prospective comparative study of intermediate-field MR and CT in the evaluation of closed head trauma. AJNR Am J Neuroradiol. 1988;9:91-100. and AJR Am J Roentgenol 150:673–682, 1988

Neuroradiology: THE REQUISITES, 2nd ed, pp 86, 88, 152–156, 174–177, 248–251, 261–262.

Comment

Acute subdural hematomas in young patients are usually the result of closed head injury (eg, motor vehicle accident), as in this case. This case shows a large right convexity, acute, actively bleeding subdural hematoma with right-to-left subfalcine herniation complicated by an acute right anterior cerebral artery infarct due to compression of this vessel. The heterogeneous “swirling” appearance within the subdural hematoma is due to active bleeding in this case, but such an appearance can also be related to leakage of serum from the clot in coagulopathic patients or patients receiving anticoagulation therapy. Also noted is subarachnoid blood and left frontal contusion.

Subdural hematomas are typically caused by tearing of the bridging veins that cross the subdural compartment, extending from the pia to the venous sinuses. Tearing of these veins is due to motion of the brain relative to the fixed dural sinuses. Most subdural hematomas are located along the supratentorial convexities; however, they may also occur in the posterior fossa and along the tentorium cerebelli.

Imaging features of subdural hematomas on CT scans depend on their age. Acute (hours to days old) hematomas are typically hyperdense “crescentic” extracerebral collections. Subacute (days to weeks old) hematomas tend to be isodense to gray matter; therefore, it is easy to miss them on a quick glance at a CT scan. To avoid missing this finding, compare the size of the sulci over the left and right cerebral convexities. Absence of sulci or asymmetric sulci should raise suspicion. Always check that the sulci extend to the inner table of the calvarium, and evaluate the gray–white matter interface for inward buckling. Chronic (weeks to months old) hematomas are usually hypodense. Fluid levels within these hematomas may be caused by interval bleeding. Calcification along the dural membrane may also occur.

Notes

CASE 18 Acute Subarachnoid Hemorrhage—Rupture of an Anterior Communicating Artery Aneurysm

1. What is the diagnosis?

2. What are common anatomic variants associated with aneurysms arising from the anterior communicating artery?

3. At what time after an acute subarachnoid hemorrhage is symptomatic vasospasm most likely to occur?

4. Aneurysms arising from what arteries may be associated with an acute-onset pupil involving third nerve palsy?

1. Acute subarachnoid hemorrhage with rupture of an anterior communicating artery aneurysm.

CASE 18

2. A hypoplastic A1 segment is most common. Other anatomic variants include duplication or fenestrations of the anterior communicating artery and azygous variation of the anterior cerebral arteries.

3. Between the fifth and twelth days.

4. The posterior communicating artery, and less frequently, the superior cerebellar artery. Pupillary dilation, ptosis, and strabismus may be present due to compression of cranial nerve III.

Jayaraman MV, Mayo-Smith WW, Tung GA, et al. Detection of intracranial aneurysms: multi-detector row CT angiography compared with DSA. Radiology. 2004;230:510-518.

Klisch J, Weyerbrock A, Spetzger U, Schumacher M. Active bleeding from ruptured aneurysms during diagnostic angiography: emergency treatment. AJNR Am J Neuroradiol. 2003;24:2062-2065.

Neuroradiology: THE REQUISITES, 2nd ed, pp 227–230.

Comment

Saccular (berry) aneurysms represent focal vascular dilations most commonly found at branching points of parent vessels. They are the result of a congenital weakness or deficiency in the elastica and media of the arterial wall. The most frequent sites for ruptured aneurysms include, in descending order of frequency, the anterior communicating artery complex, the origin of the posterior communicating artery, the middle cerebral artery, and the vertebrobasilar circulation. Multiple aneurysms may be present in up to 15% to 20% of cases. Although most aneurysms are sporadic in nature, there is an increased incidence in certain conditions, such as connective tissue disorders or collagen vascular disease (fibromuscular dysplasia, moyamoya disease, Ehlers-Danlos syndrome, and polycystic kidney disease).

The most common clinical presentation of acute subarachnoid hemorrhage is “the worst headache of my life.” Acute high-density subarachnoid blood is present on CT in 90% to 95% of cases in the first 24 hours. The sensitivity of CT in detecting acute subarachnoid hemorrhage decreases with time. Detection drops to 80% within 3 days, and to only 30% by 2 weeks. If CT is negative and acute subarachnoid hemorrhage is suspected, a lumbar puncture is performed. Evaluation of a patient with suspected acute subarachnoid hemorrhage should always begin with an unenhanced CT head study.

Patterns of intracranial hemorrhage seen with rupture of anterior communicating artery aneuryms include bilaterally symmetric subarachnoid hemorrhage, hemorrhage within the interhemispheric fissure, frontal lobe hematoma, or septal or intraventricular hemorrhage. This case shows bilaterally symmetric diffuse acute subarachnoid hemorrhage, most notably in the sylvian cisterns and basilar cisterns in a pattern consistent with rupture of an anterior communicating artery aneurysm. There is intraventricular blood and early hydrocephalus. The CT angiography source and maximum intensity projection images show a small aneurysm arising from the anterior communicating artery arising from the junction with the left A1 segment.

Notes

CASE 19 Embolic Infarcts (Acute and Subacute)—Atrial Fibrillation

Min WK, Kim YS, Kim JY, Park SP, Suh CK. Atherothrombotic cerebellar infarction: vascular lesion-MRI correlation of 31 cases. Stroke. 1999;30:2376-2381.

Neuroradiology: THE REQUISITES, 2nd ed, pp 174–176.

Comment

Approximately 80% of strokes are ischemic. They can develop in major blood vessels, referred to as “large vessel infarcts,” or in small blood vessels, perforating arteries deep in the brain and referred to as “lacunar infarcts.” Types of ischemic stroke include embolic infarct, thrombotic infarct, and lacunar infarct. Infarcts of undetermined etiology may account for as many as 30% of cases of stroke.

Cardiac embolism, in which a blood clot forms in the heart and travels to a vessel supplying the brain, accounts for about 20% to 30% of ischemic strokes. Recurrent strokes are most common in patients with a cardioembolic source, and these strokes have the highest 1-month mortality rate. Thrombotic infarcts account for 10% to 15% of strokes and occur when a blood clot forms in an artery that supplies the brain, causing tissue death. These usually occur as a result of plaque buildup from atherosclerosis and develop over time. Lacunar infarctions account for 20% of strokes, and usually occur as a result of small arterial blockage, most often caused by high blood pressure. Lacunar infarcts have a predilection for the basal ganglia, internal capsule, thalamus, pons, and corona radiata. This type of stroke has the best prognosis.

A transient ischemic attack (TIA), defined as a transient neurologic disturbance that usually persists for less than 15 minutes and resolves within 24 hours, is a risk factor for ischemic stroke. In a TIA, arterial blockage occurs briefly and resolves on its own, without causing tissue injury. Approximately 10% of ischemic strokes are preceded by a TIA, and approximately 40% of patients who experience a TIA will have a stroke.

Notes

CASE 20 Vestibular Schwannomas of the Internal Auditory Canal

Salzman KL, Davidson HC, Harnsberger HR, Glastonbury CM, Wiggin RH, Ellul S. Dumbbell schwannomas of the internal auditory canal. AJNR Am J Neuroradiol. 2001;22:1368-1376.

Neuroradiology: THE REQUISITES, 2nd ed, pp 106–107.

Comment

Schwannomas arise most commonly along sensory nerves. In the intracranial compartment, cranial nerve VIII is most commonly involved, with neuromas of the superior vestibular nerve being slightly more common than those of the inferior vestibular nerve. Schwannomas of the cochlear nerve are less common. The vestibular branches run in the superior and inferior portions of the posterior internal auditory canal (IAC), whereas the cochlear division runs in the anteroinferior portion of the IAC. Cranial nerves V (trigeminal) and VII (facial) are the next most common sites for schwannomas. When masses involve the IAC or the cerebellopontine angle (CPA), the role of the radiologist is usually in distinguishing a schwannoma from a meningioma because this may affect management. Imaging findings favoring a schwannoma are masses that involve both the cerebellopontine angle and IAC, associated flaring or widening of the porus acousticus (the opening of the IAC), and the absence of dural enhancement. Meningiomas infrequently (5%) extend into the IAC, and when they do, the IAC is not expanded and the enhancement pattern is that of peripheral enhancement “tram-tracking,” rather than centrally, as is seen with schwannomas. Meningiomas arising in the CPA may have an associated dural tail (although a dural tail is not diagnostic of a meningioma), and they are usually centered superior or inferior and anterior or posterior to the porus acousticus. In these cases, an enhancing mass involving both the IAC and the CPA (Case A), and a purely intracanalicular tumor with extension to the cochlear aperture (Case B) favor schwannomas.

Schwannomas account for more than 90% of purely intracanalicular lesions. However, only 5% to 15% are located exclusively within the IAC, whereas approximately 15% of vestibular schwannomas present only in the cerebellopontine angle cistern. Approximately 75% of these schwannomas involve both structures. On MR imaging, schwannomas have variable signal intensity, depending on their cellularity, water content, and the presence of necrosis or cystic degeneration. Small lesions (<2 cm) typically are isointense to white matter, and enhancement is often homogeneous, as in these cases. Lesions larger than 2 cm frequently undergo necrosis or cystic degeneration, resulting in heterogeneous enhancement.

Notes

CASE 21 Orbital Cellulitis and Abscess

Caruso PA, Watkins LM, Suwansaard P, et al. Odontogenic orbital inflammation: clinical and CT findings: initial observations. Radiology. 2006;239:187-194.

Neuroradiology: THE REQUISITES, 2nd ed, pp 504–505, 508–509.

Comment

It is important to distinguish orbital cellulitis that is a medical emergency from preseptal cellulitis. There are many superficial similarities between the two diseases, including lid edema and redness, and pronounced pain on palpation. However, orbital cellulitis manifests with proptosis and extraocular muscle restriction, whereas preseptal cellulitis does not. Also, patients with orbital cellulitis have fever and frequently have decreased vision. Proptosis develops due to intraorbital or postseptal abscess. Ophthalmoplegia results from toxic myopathy and soft tissue edema. Visual loss may occur due to increased intraorbital pressure from abscess and inflammation compressing the optic nerve. There typically will be a precipitating factor, such as sinusitis, penetrating lid trauma, odontogenic infection, or facial trauma. The patient may be systemically ill and have a fever. Orbital cellulitis results from microbial infection with subsequent inflammation of the postseptal orbital tissues. Common organisms include Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Haemophilus influenzae in children. There is significant potential morbidity and even mortality as a postseptal lid infection can spread through a valveless venous system, leading to cavernous sinus thrombosis, meningitis, and brain abscess.

Often, the degree of proptosis in orbital cellulitis cannot be readily appreciated due to the extreme lid edema. For this reason, CT or MR imaging may be useful not only to identify orbital abscesses, but also to ascertain precipitating sinus involvement and to exclude intracranial extension. Management involves immediate hospitalization with inpatient parenteral antibiotic therapy.

Notes

CASE 22 Acute Hypertensive Thalamic Hemorrhage

Chan S, Kartha K, Yoon SS, Desmond DW, Hilal SK. Multifocal hypointense cerebral lesions on gradient-echo MR are associated with chronic hypertension. AJNR Am J Neuroradiol. 1996;17:1821-1827.

Tanaka A, Ueno Y, Nakayama Y, Takano K, Takebayashi S. Small chronic hemorrhages and ischemic lesions in association with spontaneous intracerebral hematomas. Stroke. 1999;30:1637-1642.

Neuroradiology: THE REQUISITES, 2nd ed, pp 216–219.

Comment

This case shows a typical acute left thalamic hypertensive hemorrhage with intraventricular extension. The hematoma is mildly hypointense to brain on T1W imaging and markedly hypointense on T2W imaging. Also noted are extensive sequelae of small vessel ischemic disease in the deep periventricular white matter and in the deep gray matter of the basal ganglia. In adults, the most common cause of intracerebral hemorrhage is hypertension, which accounts for approximately 80% of nontraumatic hemorrhages. Hemorrhages related to high blood pressure have a predilection to involve the deep gray matter (basal ganglia and thalamus) and brainstem, which are supplied by perforating vessels arising from the cerebral and basilar arteries. Rupture of microaneurysms (Charcot-Bouchard) arising from the deep perforating vessels may be the basis of hypertensive hemorrhages in a subset of patients. Approximately two thirds of hypertensive hemorrhages occur in the basal ganglia. Rupture into the ventricular system, as in this case, may be present in up to one half of these patients and is associated with a poorer prognosis.

The MR imaging evaluation of intracerebral hemorrhage is complex, and the imaging appearance is related to a multitude of factors. In hyperacute hemorrhage (within the first 6 hours and rarely captured on MR imaging), hemorrhage is hypointense to brain on T1W imaging and hyperintense on T2W imaging due to oxyhemoglobin in intact red blood cells. In the acute setting (hours to a few days), as in this case, hemorrhage may be isointense to hypointense to brain on T1W and is markedly hypointense on T2W images because of increasing deoxyhemoglobin. The microenvironment of the hematoma is such that oxyhemoglobin molecules rapidly deoxygenate to deoxyhemoglobin. In the early subacute phase (2 days to 1 week), hemorrhage is hyperintense on T1W imaging and hypointense on T2W imaging as a result of high protein concentrations and intracellular methemoglobin. In the late subacute phase (1 week to months), hemorrhage is hyperintense on both T1W and T2W imaging. Finally, in the chronic setting (months to years), hemorrhage is hypointense due to susceptibility effects of hemosiderin and ferritin.

Notes

CASE 23 Infiltrating Astrocytoma—Low Grade

1. What is the differential diagnosis based on the first two images, the axial FLAIR and the corresponding enhanced axial T1W image? The patient’s history is new-onset seizure.

2. The diffusion-weighted image makes what diagnosis less likely?

3. What finding on the enhanced images makes a glial neoplasm most likely?

4. What are the three subtypes of infiltrating astrocytic neoplasms?

1. Primary glial neoplasm, metastatic disease, and infection or abscess.

CASE 23

2. Brain abscess; however, it is important to recognize that not all abscesses have restricted diffusion.

3. On the enhanced image at the level of the left insula, the left insular gray matter is expanded and nonenhancing, consistent with infiltrating neoplasm.

4. According to the World Health Organization (WHO) classification, infiltrating astrocytic tumors may be divided into three subtypes: astrocytoma, anaplastic astrocytoma, and glioblastoma multiforme (GBM).

Bagley LJ, Grossman RI, Judy KD, et al. Gliomas: correlation of magnetic susceptibility artifact with histologic grade. Radiology. 1997;202:511-516.

Preul C, Kuhn B, Lang EW, Mehdorn HM, Heller M, Link J. Differentiation of cerebral tumors using multi-section echo planar MR perfusion imaging. Eur J Radiol. 2003;48:244-251.

Neuroradiology: THE REQUISITES, 2nd ed, pp 128–129, 139, 142-–143.

Comment

According to the WHO classification, infiltrating astrocytic tumors may be divided into three subtypes: astrocytoma, anaplastic astrocytoma, and GBM. The histologic criteria for these subdivisions depend on many factors, including cellular density, number of mitoses, presence of necrosis, nuclear or cytoplasmic pleomorphism, and vascular endothelial proliferation. GBM typically has all of these histologic features, whereas the lower-grade astrocytomas may only demonstrate minimal increased cellularity and cellular pleomorphism. The presence of necrosis and vascular endothelial proliferation in particular favor GBM, the most malignant of the glial neoplasms.

Astrocytomas are CNS neoplasms in which the predominant cell type is derived from an astrocyte. Two classes of astrocytic tumors are recognized: those with narrow zones of infiltration (pilocytic astrocytoma, subependymal giant cell astrocytoma, pleomorphic xanthoastrocytoma) and those with diffuse zones of infiltration (eg, low-grade astrocytoma, anaplastic astrocytoma, GBM). The latter group may diffusely infiltrate contiguous and distant CNS structures, regardless of histologic stage, and they have a tendency to progress to more advanced grades. Regions of a tumor demonstrating the greatest degree of anaplasia are used to determine the histologic grade of the tumor.

Low-grade infiltrating astrocytomas correspond to WHO grade II, and they grow slowly compared with their malignant counterparts, anaplastic astrocytomas. Several years can intervene between initial symptoms and establishment of the diagnosis of low-grade astrocytoma. Seizures, often generalized, are the initial presenting symptom in approximately one half of patients with low-grade astrocytoma.

Notes

CASE 24 Arachnoid Cyst

Sze G. Diseases of the intracranial meninges: MR imaging features. AJR Am J Roentgenol. 1993;160:727-733.

Neuroradiology: THE REQUISITES, 2nd ed, pp 413–417.

Comment

Most intracranial arachnoid cysts are congenital and are derived from the meninx primitiva, which envelops the developing CNS. As CSF fills the subarachnoid spaces, the meninx is resorbed. At the same time, a cleft may develop between layers of the arachnoid membrane and may behave as a one-way ball-valve mechanism. There is preferential flow of CSF into this cleft, resulting in formation of a cyst. Less commonly, arachnoid cysts may be acquired as a result of adhesions in the subarachnoid space related to a previous inflammatory process or hemorrhage.

The most common location for an arachnoid cyst is the middle cranial fossa. Other common locations include the cerebral convexities (most commonly, the frontal convexity, as in this case), the basal cisterns (suprasellar, cerebellopontine angle, and quadrigeminal), and the retrocerebellar region. On CT and MR imaging, arachnoid cysts usually follow the density or intensity of CSF, respectively. When large enough, cysts may cause smooth remodeling of the inner table of the bony calvarium and osseous expansion, as is seen of the greater wing of the sphenoid in Case B. There may also be hypogenesis of the underlying brain parenchyma (most commonly described in the temporal lobe with middle cranial fossa cysts). Calcification is unusual, and enhancement should not be present.

The major differential consideration is an epidermoid cyst. On unenhanced T1W images, an internal matrix, although subtle, is typically evident in epidermoid cysts. On FLAIR images, arachnoid cysts follow the signal intensity characteristics of CSF, whereas epidermoid cysts tend to be hyperintense relative to CSF. In addition, on diffusion-weighted images, arachnoid cysts are hypointense (similar to the CSF in the ventricles), resulting from an increased apparent diffusion constant, whereas epidermoid cysts do not have an increased apparent diffusion constant.

Notes

CASE 25 Retinoblastoma

Brisse HJ, Lumbroso L, Freneaux PC, et al. Sonographic, CT, and MR imaging findings in diffuse infiltrative retinoblastoma: report of two cases with histological comparison. AJNR Am J Neuroradiol. 2001;22:499-504.

Tateishi U, Hasegawa T, Miyakawa K, Sumi M, Moriyama N. CT and MRI features of recurrent tumors and second primary neoplasms in pediatric patients with retinoblastoma. AJR Am J Roentgenol. 2003;181:879-884.

Neuroradiology: THE REQUISITES, 2nd ed, pp 479–482.

Comment

Retinoblastoma represents the most common intraocular tumor in childhood. The typical clinical presentation is leukokoria, an abnormal pupillary reflex characterized by a “white” pupil. Other common clinical presentations include strabismus, decreased visual acuity, and eye pain (which may be related to glaucoma). The majority of retinoblastomas (98%) present before 3 years of age. Retinoblastomas most commonly represent isolated sporadic tumors; however, they may be heritable in an autosomal dominant pattern. Up to 30% to 40% of patients with retinoblastoma have bilateral tumors; familial disease should be considered in these cases.

Because the radiologic hallmark of retinoblastoma is the presence of intraocular calcification before the age of 3 years, CT remains the best imaging modality for the detection of retinoblastoma. CT is also important in assessing the other eye for small calcifications. MR imaging is not as sensitive in detecting calcification. This case shows a small retinoblastoma of the right eye with restricted diffusion. Not all retinoblastomas (particularly small ones) have calcification, so the absence of calcification does not exclude the possibility of retinoblastoma. MR imaging plays an important role in assessing these patients because retinoblastoma may spread along the nerves and vessels to the retrobulbar orbit, and there may be subarachnoid seeding. Both modes of transmission may result in intracranial dissemination of disease. Therefore, patients with retinoblastoma should be evaluated with MR imaging to determine the extent of disease. A small percentage (<5%) of patients with bilateral retinoblastomas may also have a pineoblastoma of the pineal gland (“third eye”).

Notes

CASE 26 Subdural Empyema—Complicated by Cerebritis

Fountas KN, Duwayri Y, Kapsalaki E, Dimopoulos VG, Johnston KW, Peppard SB. Epidural intracranial abscess as a complication of frontal sinusitis: case report and review of the literature. South Med J. 2004;97:279-282.

Neuroradiology: THE REQUISITES, 2nd ed, pp 274, 276–277.

Comment

Interruption of the arachnoid meningeal barrier by infection leads to the formation of subdural empyemas. Mechanisms by which subdural empyemas may develop include rupture of a distended arachnoid villus into the subdural compartment, thrombophlebitis of a bridging cortical vein, hematogenous spread, and direct spread of an extracranial infection (sinusitis, otomastoiditis, osteomyelitis). These serious infections may also occur as a complication after craniotomy or in patients with meningitis. Epidural abscesses are most frequently caused by direct extension of infection from the paranasal sinuses or mastoid air cells. Of conditions affecting the paranasal sinuses, frontal sinusitis is probably the most common cause of intracranial epidural abscesses and subdural empyemas.

On imaging, these lesions share the common appearance of other extracerebral collections. Epidural abscesses (like hematomas) are contained by the cranial sutures and may cross the midline. In contrast, subdural hematomas do not spread across the midline because they are confined by the falx, allowing differentiation from epidural collections. On MR imaging, these extracerebral infections are usually hypointense to isointense on T1W imaging (depending on the protein concentration and the cellular content) and hyperintense relative to the brain on FLAIR and T2W imaging. Empyemas typically are hyperintense on diffusion-weighted imaging (DWI) and have low apparent diffusion coefficients (ADCs), as in this case, whereas sterile subdural effusions are hypointense on DWI. There is usually prominent enhancement of thickened dura or a dural membrane. Epidural and subdural empyemas may be complicated by cerebritis (as in this case) and intraparenchymal abscess formation. In addition, dural venous or cortical vein thrombosis with venous infarction may occur. In the presence of suspected epidural abscess or subdural empyema, the radiologist (and the clinician!) should search for a site of origin of the infection, as well as its contiguous spread into the intracranial compartment.

Notes

CASE 27 Glioblastoma Multiforme of the Corpus Callosum—”Butterfly Glioma”

1. What mass lesions have a predilection for involving the corpus callosum?

2. Why is the corpus callosum relatively resistant to edema?

3. What white matter tracts are common conduits of spread of glial neoplasms from one cerebral hemisphere to the contralateral side?

4. What are the MR imaging findings of gliomatosis cerebri?

1. Neoplasms (glioblastoma multiforme, lymphoma, and much less commonly, metastatic disease), demyelinating disease, and traumatic shear injury.

CASE 27

2. The corpus callosum is relatively resistant to edema because of the orientation and compact nature of the white matter fibers forming it.

3. The corpus callosum and the anterior and posterior commissures.

4. Gliomatosis cerebri is uncommon and refers to an extensive infiltrating glioma with imaging findings that are usually out of proportion to those on histologic evaluation and clinical examination. MR imaging shows extensive involvement of both the gray and white matter, with mild diffuse sulcal and ventricular effacement. There is often minimal or no enhancement of involved areas.

Rees JH, Smirniotopoulos JG, Jones RV, Wong K. Glioblastoma multiforme: radiologic-pathologic correlation. RadioGraphics. 1996;16:1413-1438.

Neuroradiology: THE REQUISITES, 2nd ed, pp 139, 142–143.

Comment

This case demonstrates findings characteristic of a butterfly glioma. There is a complex extensive mass with expansion of the splenium and body of the corpus callosum. Abnormal signal intensity and multiple more defined areas of necrotic mass are noted. Enhanced images better reveal the marked necrosis of certain portions of the tumor. Ventricular ependymal enhancement is shown (*).

Multicentric gliomas are uncommon, occurring in 1% to 5% of cases of GBM. They may represent true separate lesions; however, more often they represent contiguous spread of tumor (which is the case in this patient). Multicentric gliomas may be synchronous (multiple lesions detected at the time of presentation) or metachronous (occurring at different times and pathologically discontinuous). It may occasionally be difficult to distinguish such gliomas from metastases on imaging. When separate lesions are identified, it is important to evaluate for the presence of continuity between the separate lesions on the basis of abnormal T2W signal intensity. However, the connection may not be apparent on imaging and may be seen only on pathologic evaluation. There is an increased association of multicentric gliomas in neurofibromatosis type I. In this case, a thin rind of ependymal enhancement is present along the body of the right lateral ventricles just medial to the (*). Of the infiltrative astrocytic tumors, GBM is most commonly associated with subependymal and ependymal spread.

Notes

CASE 28 Virchow-Robin Perivascular Spaces

Song CJ, Kim JH, Kier EL, Bronen RA. MR imaging and histologic features of subinsular bright spots on T2-weighted MR images: Virchow-Robin spaces of the extreme capsule and insular cortex. Radiology. 2000;214:671-677.

Neuroradiology: THE REQUISITES, 2nd ed, pp 345–346.

Comment

This case illustrates the typical appearance of a Virchow-Robin perivascular space. Diagnostic considerations for deep basal ganglia lesions primarily include chronic lacunar infarcts; however, developmental cysts, cystic neoplasms, and occasionally chronic infections could potentially share many of the same imaging features. Dilated perivascular spaces can usually be distinguished from a lacunar infarct on the basis of typical imaging findings. Lacunar infarcts tend to occur in the upper half of the putamen, whereas perivascular spaces occur along the inferior half. In addition, whereas perivascular spaces are usually isointense to CSF on all pulse sequences, this is not the case with lacunar infarcts unless they have undergone cystic degeneration. Even when cystic, lacunar infarcts may have a thin surrounding hyperintense rim on T2-weighted and FLAIR images, representing gliosis. Dilated perivascular spaces are not associated with edema or enhancement, have a characteristic location along the anterior commissure, and are frequently bilateral and symmetric (as in Case B). In addition to the basal ganglia, they also frequently occur in the cerebral peduncles, in the subinsular white matter, and in the white matter lateral to and above the lateral ventricles. Frequently, a vessel can be seen coursing through these spaces, as in Case A.

Perivascular spaces are extensions of the subarachnoid space that follow the perforating vessels at the base of the brain into the basal ganglia. Virchow-Robin spaces may range from 1 to 15 mm in size, although occasionally they can be larger. They tend to enlarge with age and in the presence of hypertension. This makes sense because most vessels (including those along the perivascular spaces) become more ectatic under both of these circumstances. In addition, just as the subarachnoid spaces become more prominent with age in that the perivascular spaces are extensions of the subarachnoid space, it makes sense that they enlarge in a similar manner. Given the extension of the perivascular spaces from the subarachnoid space into the brain, they are a conduit for the spread of a variety of inflammatory and neoplastic processes (eg, Cryptococcus, sarcoid, carcinomatosis). Incidentally noted are cysts of the choriod plexus (*).

Notes

CASE 29 Agenesis of the Corpus Callosum

1. What are the names of these structures (arrows)?

2. The course of the mesial hemispheric sulci is uninterrupted in a radial manner all the way to the third ventricle because of the absence of what structure?

3. What congenital anomalies are associated with this entity?

4. In primary partial dysgenesis of the corpus callosum, which portions of the corpus callosum are typically spared?

1. The Probst bundles are the white matter tracts that were destined to cross the corpus callosum. The axons that would usually cross from right to left in the corpus callosum instead form tracts that run anterior to posterior along the medial walls of the lateral ventricles parallel to the interhemispheric fissure.

CASE 29

2. The cingulate gyrus.

3. Lipomas, migrational abnormalities, Dandy-Walker syndrome, Chiari malformations, and holoprosencephaly, to name just a few!

4. The anterior portions (except the rostrum).

Lee SK, Mori S, Kim DJ, Kim SY, Kim SY, Kim DI. Diffusion tensor MR imaging visualizes the altered hemispheric fiber connection in callosal dysgenesis. AJNR Am J Neuroradiol. 2004;25:25-28.

Quigley M, Cordes D, Turske P, Moritz C, Haughton V, Seth R. Role of the corpus callosum in functional connectivity. AJNR Am J Neuroradiol. 2003;24:208-212.

Neuroradiology: THE REQUISITES, 2nd ed, pp 424–425.

Comment

Axons arising from the right and left cerebral hemispheres grow into the lamina reuniens (the dorsal aspect of the lamina terminalis), giving rise to the corpus callosum (and the hippocampal commissures). The corpus callosum develops between the 11th and 20th gestational weeks in an organized manner, with formation of the anterior genu first followed in order by the anterior body, posterior body, splenium, and rostrum. Given this pattern of development, in partial dysgenesis of the corpus callosum, the anterior portion is formed and partial dysgenesis affects the posterior portions (posterior body, splenium) and rostrum. In cases in which the splenium is very small or is not visualized, partial dysgenesis of the corpus callosum can be readily distinguished from an insult to a previously fully developed splenium by checking for the presence of the rostrum. If the rostrum is absent, the splenial abnormality corresponds to partial dysgenesis. However, if the rostrum is present, given that it forms after the splenium, a splenial abnormality must have occurred on the basis of an insult resulting in secondary atrophy or volume loss.

Imaging findings in complete agenesis of the corpus callosum include lack of convergence of the lateral ventricles, which are displaced laterally and oriented in a vertical fashion; a high-riding third ventricle (which may form an interhemispheric cyst); and ex vacuo enlargement of the occipital and temporal horns (colpocephaly) related to deficient white matter. The Probst bundles are the white matter tracts that were destined to cross the corpus callosum. The axons that would usually cross from right to left in the corpus callosum instead form tracts that run anterior to posterior along the medial walls of the lateral ventricles parallel to the interhemispheric fissure.

Notes

CASE 30 Nonaccidental Trauma—Child Abuse

Demaerel P, Casteels I, Wilms G. Cranial imaging in child abuse. Eur Radiol. 2002;12:849-857.

Mogbo KI, Slovis TL, Canady AI, Allasio DJ, Arfken CL. Appropriate imaging in children with skull fractures and suspicion of abuse. Radiology. 1998;208:521-524.

Neuroradiology: THE REQUISITES, 2nd ed, pp 264–266.

Comment

The presence of skull fractures or intracranial hemorrhage, particularly in children younger than the age of 2 years, in the absence of known trauma to explain such injuries, should raise the suspicion of child abuse (nonaccidental trauma). There are more than 1 million reported cases of child abuse each year, and closed head injury is among the leading causes of morbidity and death in these children. Approximately 10% of neurologic developmental delays can be attributed to nonaccidental trauma. Brain injury may be the result of direct trauma, aggressive shaking, or strangulation or suffocation. There is often little or no evidence of external trauma.

The most common type of intracranial hemorrhage in the setting of child abuse is a subdural hematoma, although subarachnoid hemorrhage, epidural hematoma, intraventricular hemorrhage, hemorrhagic cortical contusion, and diffuse axonal injury are all manifestations of nonaccidental trauma. Bilateral retinal hemorrhages are highly suggestive of child abuse (shaken baby syndrome). In the absence of significant head trauma, the presence of skull fractures (especially bilateral, depressed, or occipital fractures), which are found in as many as 45% of nonaccidental trauma cases, should raise suspicion for child abuse. Because it is not fully developed, the infant skull is extremely pliable and relatively resistant to fracture. In the worse case, diffuse cerebral edema resulting in mass effect and herniation may occur in nonaccidental trauma. Cerebral infarction may occur as a result of strangulation or anoxic-hypoxic injury, and vascular compromise may be caused by intracranial mass effect. Infarctions in multiple vascular territories should be viewed with suspicion.

The radiologist plays an important role in identifying nonaccidental head trauma. The clinical presentation can be nonspecific. The radiologist is sometimes in a position to suggest the possibility of child abuse. It is therefore important to know the spectrum of sometimes subtle imaging findings that may be encountered. Skull x-ray and head CT are regularly used. Repeat or serial imaging may be necessary. Brain MR imaging may contribute to the diagnostic workup, particularly in the absence of characteristic CT findings.

Notes

CASE 31 Dermoid Cysts

1. What substances are hyperintense on unenhanced T1W imaging?

2. On MR imaging, what artifact is indicative of the presence of fat?

3. What lesions on imaging may contain both fat and calcium?

4. What causes chemical shift artifact?

1. Fat, proteinaceous material, methemoglobin (hemorrhage), manganese, some calcium, liquid cholesterol, pantopaque contrast, and melanin.

CASE 31

2. Chemical shift artifact. Fat is hyperintense on fast spin echo T2W images. When there is a question, fat suppressed T1W imaging may confirm the presence of fat.

3. Dermoid cysts and teratomas. Lipomas may occasionally have calcification; however, this is less common than with teratomas and dermoid cysts. Calcification may be seen with “tumefactive” lipomas in the interhemispheric fissure that are usually associated with dysgenesis of the corpus callosum, allowing differentiation from dermoid cysts and teratomas.

4. Fat and water precess at slightly different Larmor frequencies (fat precesses more slowly). For correct spatial localization, the Larmor frequency must be uniform throughout the section. Chemical shift artifact results because the position of fat protons relative to water is altered during frequency encoding because its signal is assumed to originate from an incorrect location. Chemical shift artifact on long TR images is identified by the presence of a hyperintense rim and a hypointense rim at opposite margins of the lesion in the frequency encoding direction.

Calabro F, Capellini C, Jinkins JR. Rupture of spinal dermoid tumors with spread of fatty droplets in the cerebrospinal fluid pathways. Neuroradiology. 2000;42:572-579.

Neuroradiology: THE REQUISITES, 2nd ed, pp 116, 543–544.

Comment

Epidermoid and dermoid lesions are developmental anomalies that may be considered congenital inclusions within the neural tube related to incomplete dysjunction of the neuroectoderm from the cutaneous ectoderm. Both lesions are of epidermal origin and may be associated with dermal sinuses or a bone defect. Dermoid cysts and teratomas are typically midline lesions, and both occur more commonly in men. In the intracranial compartment, they may be found in the parasellar or suprasellar region (as in Case B), frontal or basal surface of the brain, and in the posterior fossa. Within the posterior fossa, the superior cerebellar cistern (as in Case A) and fourth ventricular regions are the most common locations.

On CT, dermoids are decreased in attenuation (<−120 Hounsfield units) because of their fat content. Calcification may be seen in the periphery of the lesion. On MR imaging dermoids show the signal characteristics of fat, and chemical shift artifact is frequently present. When necessary, fat suppression can be applied to confirm the diagnosis. Compare the first image in Case A, which is an unenhanced T1W image, with the second image, which is an unenhanced T1W image with frequency selective fat saturation applied. Other common MR imaging findings in these relatively uncommon lesions include the presence of fat-fluid levels within dermoid cysts, and peripheral enhancement. On the other hand, teratomas often have areas of solid enhancement.

Dermoid cysts may contain dermal appendages, including sebaceous and sweat glands, as well as hair follicles. They are often asymptomatic but may enlarge over time due to recurrent glandular secretions and/or recurrent desquamation of the epithelial lining of the cyst. When symptomatic, patients may have headaches. A serious complication of dermoid cysts is their propensity to rupture into the subarachnoid space (as in Case A), which may result in an inflammatory chemical meningitis, vasospasm with ischemia, and even death. It is important on imaging to check for fat droplets within these locations.

Notes

CASE 32 Calvarial Metastases—Breast Carcinoma

Loevner LA, Tobey JD, Yousem DM, Sonners AI, Hsu WC. MR imaging characteristics of cranial bone marrow in adults with underlying systemic disorders compared with healthy controls. Am J Neuroradiol. 2002;23:248-254.

West MS, Russel EJ, Breit R, Sze G, Kim IKS. Calvarial and skull base metastases: comparison of nonenhanced and Gd-DTPA-enhanced MR images. Radiology. 1990;174:85-91.

Neuroradiology: THE REQUISITES, 2nd ed, p 149.

Comment

This case shows mixed blastic and lytic metastases in a patient with breast carcinoma. Prostate carcinoma is the most common cause of blastic metastases in men. Other carcinomas that may present with blastic metastases include breast carcinoma (as shown here) and, less commonly, carcinoid, Hodgkin’s lymphoma, and mucinous carcinomas of the lung, colon, and bladder. In older patients, blastic or mixed metastases (blastic and lytic) can be mistaken for the “cotton-wool” appearance of diffuse calvarial Paget’s disease. On close examination of a CT scan, these can often be distinguished. In addition to having regions of sclerosis or lysis, Paget’s disease is usually associated with thickening of the diploic space, as well as cortical thickening. In contrast, metastatic disease (as in this case) is typically not associated with significant bone expansion, and usually there is not cortical thickening. In this case, there are erosion and destruction of the outer cortical table in the right frontoparietal skull (not cortical thickening), suggesting a more aggressive process.

When there is a question about the diagnosis, particularly in a patient without a known systemic malignancy, a bone scan may be performed. In most instances, both pagetoid bone and metastatic disease will be “hot”; however, the reason to perform the bone scan is not to assess the skull, but rather to assess the remainder of the skeleton for evidence of additional foci of metastatic disease. Paget’s disease is not infrequently polyostotic (involving multiple sites); however, plain radiographs of additional pagetoid lesions detected on bone scans usually have a characteristic appearance.

Notes

CASE 33 Chronic Anemia—Diffuse Replacement of Fat in the Calvarial Marrow

Loevner LA, Tobey JD, Yousem DM, Sonners AI, Hsu WC. MR imaging characteristics of cranial bone marrow in adults with underlying systemic disorders compared with healthy controls. Am J Neuroradiol. 2002;23:248-254.

Ricci C, Cova M, Kang YS, et al. Normal age-related patterns of cellular and fatty bone marrow distribution in the axial skeleton: MR imaging study. Radiology. 1990;177:83-88.

Neuroradiology: THE REQUISITES, 2nd ed, p 806.

Comments

The normal signal intensity of marrow is dependent on the ratio of cells, fat, and water. In children, hematopoietic (red) marrow has a high cell:fat ratio and is hypointense. As we age, the amount of fat increases such that by early adulthood the marrow has undergone fatty conversion (yellow marrow), and on T1W images, it is isointense to hyperintense to white matter. Unenhanced T1W imaging is probably the best way to assess for marrow abnormalities, especially because it is part of all standard brain MR imaging protocols.

Hematopoietic (red) marrow is composed of approximately 40% fat, 40% water, and 20% protein; in contrast, inactive fatty (yellow) marrow contains approximately 80% fat, 10% to 15% water, and 5% protein. On unenhanced T1W images, yellow marrow has high signal intensity relative to that of muscle; it approaches the intensity of subcutaneous fat. Cellular red marrow has intermediate signal intensity and may be isointense or slightly hyperintense relative to muscle. Marrow conversion represents a normal process in which yellow marrow gradually replaces red marrow. At birth, marrow is predominantly red in both the appendicular and axial skeletons. In the appendicular skeleton, most of the marrow has undergone conversion by the time an individual is 21 years of age. Residual red marrow is found in the proximal metaphyses of the femurs and humeri. In the axial skeleton, in adults, a larger portion of the marrow remains hematopoietic compared with the appendicular skeleton.

The differential diagnosis of diffuse replacement of the fatty marrow with hypointense tissue (cells or water) includes hematologic malignancies (lymphoma, leukemia, and myeloma); granulomatous disease (sarcoid and tuberculosis); chronic anemias, such as thalassemia, sickle cell disease, or chronic blood loss; and AIDS (hypointense marrow has been attributed to several factors, including chronic anemia and low CD4 counts). Metastases may diffusely replace the marrow (most common with breast carcinoma in women and prostate carcinoma in men). More often, metastatic disease presents with multiple focal lesions.

Notes

CASE 34 Giant Aneurysm—Middle Cerebral Artery

Jayaraman MV, Mayo-Smith WW, Tung GA, et al. Detection of intracranial aneurysms: multi-detector row CT angiography compares with DSA. Radiology. 2004;230:510-518.

Neuroradiology: THE REQUISITES, 2nd ed, pp 224–230.

Comment

The middle cerebral artery bifurcation or trifurcation has a propensity for the development of giant aneurysms. Giant aneurysms may present with subarachnoid hemorrhage or symptoms caused by mass effect (nausea, vomiting, focal neurologic deficits) related to aneurysm size or intraparenchymal rupture or hematoma.

A thrombus may form within large aneurysms and may be a source of distal emboli. Unenhanced CT may show the giant aneurysm as a hyperdense mass. At its periphery there may be heterogeneous density related to the presence of thrombus. On MR imaging, giant aneurysms have a characteristic appearance, as in this case. Findings include signal void consistent with flow in the patent lumen; phase artifact related to flow, as is seen in this case; and heterogeneous signal intensity representing thrombi of varying ages.

Recent investigations with CT angiography in the setting of subarachnoid hemorrhage have shown detection rates for all aneurysms as high as 96%. False-negative findings may be related to CT angiography technique, aneurysm size (especially those < 3 mm), and aneurysm location. Aneurysms originating from the posterior communicating artery, the infraclinoid internal carotid artery, and the ophthalmic artery that are in close proximity to bone now are readily detected due to improved bone subtraction techniques. Advantages of CT angiography include its rapidity, noninvasiveness, ability to provide information about potential neuroangiographic intervention, and ability to provide preoperative information about the relationship of an aneurysm to adjacent bony landmarks. Catheter angiography is still the most commonly used technique and the accepted standard in the assessment of acute subarachnoid hemorrhage.

Notes

CASE 35 Bilateral Subacute Subdural Hematomas

Atkinson JL, Lane JI, Aksamit AJ. MRI depiction of chronic intradural (subdural) hematoma in evolution. J Magn Reson Imaging. 2003;17:484-486.

Pollo C, Meuli R, Porchet F. Spontaneous bilateral subdural haematomas in the posterior cranial fossa revealed by MRI. Neuroradiology. 2003;45:550-552.

Neuroradiology: THE REQUISITES, 2nd ed, pp 248–251.

Comment

The appearance of blood products on MR imaging is dependent on several factors, most importantly, the structure of hemoglobin at the time of imaging. Oxyhemoglobin (oxygen bound to the iron of hemoglobin) is diamagnetic because it effectively has no unpaired electrons. On giving up its oxygen, deoxyhemoglobin is formed and hemoglobin undergoes a small but significant structural change such that water molecules in the vicinity of deoxyhemoglobin are unable to bind to the iron. Deoxyhemoglobin has four unpaired electrons and may be oxidized to methemoglobin. Methemoglobin has five unpaired electrons, and water molecules are able to bind to the iron atom.

Susceptibility effects, proton–electron dipole–dipole interactions, and other factors contribute to the variable signal characteristics of blood products on MR imaging. When placed in a magnetic field, certain substances may induce an additional smaller magnetic field that may add to the externally applied field. This phenomenon may be seen with paramagnetic substances (deoxyhemoglobin and methemoglobin). Alternatively, other substances, when placed in a magnetic field, may induce magnetic fields that subtract from the externally applied field (seen with diamagnetic materials, such as oxyhemoglobin). Susceptibility effects of blood products depend on the proportionality constant between the strength of the applied magnetic field and the induced magnetic field.

Methemoglobin induces a local magnetic field significantly greater than that of a proton. Therefore, if a proton gets close enough to this field, a spin transition may occur. To have a proton–electron dipole–dipole interaction, water must bind to heme. Even though the number of heme molecules is small relative to that of water, the exchange rate of water molecules is quite rapid compared with the repetition time; hence, many water molecules are bound to heme during MR imaging. Proton–electron dipole–dipole interactions result in shortening of T1 and T2.

Notes

CASE 36 Parafalcine Meningioma Invading the Superior Sagittal Sinus

Takeguchi T, Miki H, Shimizu T, et al. The dural tail of intracranial meningiomas on fluid-attenuated inversion-recovery images. Neuroradiology. 2004;46:130-135.

Tsuchiya K, Katase S, Yoshino A, Hachiay J. MR digital subtraction angiography in the diagnosis of meningiomas. Eur J Radiol. 2003;46:130-138.

Neuroradiology: THE REQUISITES, 2nd ed, pp 98–105, 217, 218–220.

Comment

This case shows a well-demarcated extra-axial mass (CSF cleft separating the mass from the brain on T2W image) in the posterior interhemispheric fissure along the falx cerebri. The mass is predominantly isointense to gray matter (because of its cellularity) and enhances avidly, with the exception of a few small areas of cystic degeneration (T2W hyperintense, nonenhancing regions). Enhancing tumor is noted obliterating the superior sagittal sinus (*).

In trying to determine the cause of this lesion, it is important to view the remainder of the brain as well as the calvaria for other abnormalities. This is because the vast majority of malignant extra-axial neoplasms are caused by bone metastases. Destructive or infiltrative lesions within the calvaria that may affect the inner and outer cortical tables should be sought. In addition, metastases may be associated with extraosseous soft tissue masses within the scalp. The finding of multiple lesions within the calvaria favors metastatic disease. Additional malignant extra-axial masses include metastases and lymphoma (which may involve the leptomeninges, dura, or bone). Finally, the absence of significant associated vasogenic edema in this case makes a malignant process unlikely. The opposite is not true, however; the presence of significant vasogenic edema would support meningioma or a more aggressive neoplasm (eg, metastases, lymphoma).

The most common cause of an extra-axial neoplasm in adults is meningioma. Although meningiomas may demonstrate changes along the inner table of the skull (hyperostosis and, less commonly, lysis), a dural-based mass in the absence of disease involving the diploic space or the outer table of the skull still favors meningioma (as do statistics!)

Notes

CASE 37 Hemorrhagic Venous Infarction

1. What are the two most common types of antiphospholipid antibodies?

2. In hypercoagulable states related to antiphospholipid antibodies, are cerebral arterial or venous infarcts more common?

3. What images in this case identify the presence of blood products?

4. What kidney disorder is associated with a hypercoagulable state?

1. Lupus anticoagulant and anticardiolipin. There is a high incidence of these circulating antibodies in patients with systemic lupus erythematosus.

CASE 37

2. Arterial infarcts.

3. The mass shows hyperintensity on the T1W image and mild hypointensity on the T2W image. The baseline images from the diffusion-weighted data set (T2W EPI) show more convincing decreased intensity because they are more sensitive to susceptibility effects than the relatively insensitive fast spin-echo T2W sequence. More optimal demonstration of susceptibility effects could be obtained with T2W gradient echo imaging (not acquired in this patient).

4. Nephrotic syndrome. The hypercoagulable state is multifactorial and includes the combined effects of endothelial injury, platelet hyperaggregability, and abnormalities in the coagulation cascade (such as protein S or C deficiency).

Tong KA, Ashwal S, Obenaus A, Nickerson JP, Kido D, Haacke EM. Susceptibility-weighted MR imaging: a review of clinical applications. Am J Neuroradiol. 2008;29:9-17.

Neuroradiology: THE REQUISITES, 2nd ed, pp 217, 219–220.

Comment

This case illustrates a hemorrhagic venous infarction in the left temporal lobe. Unlike arterial infarctions, the anatomic territories for venous occlusive disease are less consistent than with the territory supplied by arteries. Several findings should raise the suspicion of a venous infarct: (1) the presence of hemorrhage, especially in the white matter or at the gray–white matter interface; (2) the presence of an abnormality that is not in a single arterial distribution; and (3) an infarct in a young patient. This patient had acute thrombosis of the vein of Labbé and the distal left transverse sinus. The hemorrhagic infarct in the left temporal lobe is in the territory drained by the vein of Labbé.

Symptoms of venous occlusion are related to the rate at which collateral venous drainage is established, the location of the clot, and the rate of clot formation. Because of the network of venous collaterals in the brain, if the venous occlusive process is slow enough to allow time for collateral circulation to develop, the patient may remain asymptomatic. However, in the setting of acute occlusion of a large vein or dural venous sinus, venous congestion will result in back-pressure that extends to the capillary bed, where the flow will be diminished such that there is ischemia and, if extensive enough, infarction.

Before MR imaging and CT venography, the diagnosis of venous occlusive disease was more difficult, and a high index of suspicion was necessary. Many conventional CT findings have been described (including the delta sign, in which there is enhancement around the clot or filling defect in the sinus, and the cord sign, in which high density is seen in a venous sinus or vein); however, they are inconsistent.

Notes

CASE 38 Vertebral Artery Dissection—Spontaneous

Naggara O, Oppenheim C, Toussaint JF, et al. Asymptomatic spontaneous acute vertebral artery dissection: diagnosis by high-resolution magnetic resonance images with a dedicated surface coil. Eur Radiol. 2007;17:2434-2435.

Neuroradiology: THE REQUISITES, 2nd ed, pp 221–224, 263–264.

Comment

These MR images show narrowing of the lumen of the distal extracranial right vertebral artery (*) with surrounding mural hematoma that is hyperintense on the fat-suppressed unenhanced T1W image. Vascular dissections may be asymptomatic. When symptomatic, the symptoms may occur days to weeks after the actual injury. As a result, dissections often escape clinical detection. In addition, symptomatic lesions can be overlooked or masked by other injuries in patients with acute injuries. Therefore, the key to making the diagnosis is considering it in the appropriate clinical scenario. Although CT is not a sensitive study for detecting vascular injuries, it may identify patients at increased risk (those with skull base fractures or fractures of the vertebral bodies extending through the foramen transversarium, which houses the cervical vertebral artery). It is also important to recognize that vertebral artery dissections may be spontaneous (no clear etiology, minor trauma), and may occur in association with excessive vomiting, coughing, and excessive straining.

The combination of MR imaging and MR angiography is sensitive for detecting vascular injuries because these assess the vascular lumen, the vessel wall, and tissues around the vessel. MR imaging findings include intramural hematoma, which is typically hyperintense on unenhanced T1W images, as in this case, and narrowing and compromised flow in the arterial lumen (a narrowed but patent vessel can usually be distinguished from one that is occluded). Pseudoaneurysms may also be detected. The conventional angiographic appearance of a dissection may vary, and includes spasm, segmental tapering related to intramural hematoma (the hematoma is not visualized on angiography), aneurysmal dilation of the vessel, vascular occlusion, intimal flap, or retention of contrast material in the vessel wall.

Notes

CASE 39 Spontaneous Cerebral Hematoma—Ruptured Cerebral Arteriovenous Malformation

1. What is the differential diagnosis for a spontaneous, nontraumatic cerebral hematoma?

2. What entity would not be expected to be seen in patients younger than 60 years of age?

3. What is the cause of this young patient’s spontaneous frontal lobe hematoma?

4. What are the anatomic structures marked with (*)?

1. Hemorrhage into an underlying tumor, hemorrhage into an underlying vascular malformation (ruptured arteriovenous malformation [AVM], cavernoma), venous infarct, vasculitis, hemorrhagic arterial infarct, substance abuse (cocaine), amyloid angiopathy.

CASE 39

2. Amyloid angiopathy is usually seen in patients older than 60 years of age, and is a diagnosis of exclusion.

3. A ruptured AVM. The nidus is the tangle of blood vessels in the left frontal lobe on the conventional arteriogram.

4. Early draining veins to the superficial (*) and deep (**) venous systems.

Cloft HJ, Joseph GJ, Dion JE. Risk of cerebral angiography in patients with subarachnoid hemorrhage, cerebral aneurysm, and arteriovenous malformation. Stroke. 1999;30:317-320.

Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg. 1986;65:476-483.

Neuroradiology: THE REQUISITES, 2nd ed, pp 234–238.

Comment

This case shows a nontraumatic spontaneous hematoma in the left frontal lobe with surrounding hypodensity, consistent with edema and early clot retraction. There is local mass effect with sulcal effacement and mild posterior displacement of the frontal horn of the left lateral ventricle. There is blood in a persistent cavum vergae. In this case, the hematoma is due to a ruptured AVM. The vascular nidus is noted in the left frontal lobe. An AVM represents a vascular nidus made up of a core of entangled vessels fed by one or more enlarged feeding arteries. Blood is shunted from the nidus to enlarged draining veins that terminate in the deep or superficial venous system. In this case, there is superficial venous drainage (*) in the left frontal region that drains to the superior sagittal sinus, and there is deep venous drainage (**) to the internal cerebral veins.

On unenhanced CT, the vascular nidus of an AVM and enlarged draining veins are usually isodense or hyperdense to gray matter as a result of pooling of blood. Calcification may be present. AVMs enhance and have characteristic serpentine flow voids on MR imaging related to fast flow in dilated arteries. In lesions associated with an acute parenchymal hemorrhage, phase-contrast MR angiography best demonstrates the AVM (it subtracts out the signal intensity of the blood products in the hematoma, in contrast to time-of-flight MR angiography). Cerebral angiography shows enlarged feeding arteries, the vascular nidus, and early draining veins. In cases of very small AVMs, early venous filling should be sought on careful evaluation of the angiographic images.

Notes

CASE 40 Vascular Infundibulum—Posterior Communicating Artery

1. What is the first branch to arise from the supraclinoid internal carotid artery?

2. How does a clinician differentiate a posterior communicating artery aneurysm from an infundibulum?

3. What percentage of patients with nontraumatic subarachnoid hemorrhage will have unrevealing (negative) angiograms?

4. What are some causes of angiographically negative subarachnoid hemorrhage?

1. The ophthalmic artery.

CASE 40

2. An infundibulum should meet the following criteria: (1) it measures 3 mm or smaller; (2) it is triangular or funnel-shaped; and (3) the posterior communicating artery arises from its apex.

3. Approximately 10% to 15%.

4. Aneurysms may not be detected because of vasospasm that inhibits filling of the aneurysm, spontaneous thrombosis of the aneurysm, or misinterpretation of the images. Other causes of angiogram-negative subarachnoid hemorrhage include perimesencephalic venous hemorrhages, vasculitis, venous thrombosis, and spinal vascular malformations.

Marshman LA, Ward PJ, Walter PH, Dossetor RS. The progression of an infundibulum to aneurysm formation and rupture: case report and literature review. Neurosurgery. 1998;43:1445-1448.

Ng SH, Wong HF, Ko SF, Lee CM, Yen PS, Wai YY. CT angiography of intracranial aneurysms: advantages and pitfalls. Eur J Radiol. 1997;25:14-19.

Neuroradiology: THE REQUISITES, 2nd ed, pp 226–227.

Comment

These angiographic images demonstrate the typical appearance of a posterior communicating artery infundibulum, showing its funnel shape as well as the origin of the posterior communicating artery from the apex of the infundibulum. Because the management is dramatically different, angiographic images in anteroposterior, lateral, and oblique projections should be obtained to accurately differentiate an aneurysm from an infundibulum.

Conventional catheter angiography and, increasingly, CT angiography are used in the diagnosis and evaluation of intracranial aneurysm. In the acute setting, there are several indications for prompt imaging evaluation, including nontraumatic subarachnoid hemorrhage; acute-onset third nerve palsy that involves the pupil (to exclude a posterior communicating or superior cerebellar artery aneurysm); and in the postoperative setting, to evaluate complications after placement of an aneurysm clip. In patients with angiogram-negative acute nontraumatic subarachnoid hemorrhage, follow-up angiography is usually indicated. It is important to remember that all potential sites of aneurysm formation must be assessed with conventional angiography. In the acute setting, postoperative angiography is often indicated in the evaluation of perioperative ischemic sequelae (which may be due to embolic phenomena, vasospasm, or vascular occlusion). Postoperative or intraoperative angiography on an elective basis may be performed to assess for residual aneurysm after aneurysm clipping.

Notes

CASE 41 Closed Head Injury—Diffuse Axonal Injury

1. What are the most common locations for traumatic contusions?

2. What three anatomic locations are classically involved in diffuse axonal injury?

3. Why are the posterior and splenial regions of the corpus callosum more commonly affected by shear injury than the anterior portion?

4. In the absence of the gradient echo image, what other entities could result in similar imaging findings seen on the long TR images?

1. The frontal and temporal lobes. The anterior temporal lobes impact on the greater wing of the sphenoid bone, whereas the frontal lobes impact on the surfaces of the cribriform plate, orbits, and frontal bone.

CASE 41

2. The lobar white matter, the corpus callosum (most commonly the splenium, but also the undersurface of the posterior body), and the dorsolateral aspect of the upper brainstem (midbrain and pons).

3. With rotational acceleration of the head, shear forces develop across the corpus callosum. Anteriorly, there is less strain because the falx is shorter and allows transient displacement of the frontal lobes across the midline. Posteriorly, the falx is broader and more rigid, preventing motion of the cerebral hemispheres across the midline.

4. Demyelinating diseases (multiple sclerosis, acute disseminated encephalomyelitis) and neoplasm (primary glial and lymphoma).

Scheid R, Preul C, Gruber O, Wiggins C, von Cramon DY. Diffuse axonal injury associated with chronic traumatic brain injury: evidence from T2-weighted gradient-echo imaging at 3T. AJNR Am J Neuroradiol. 2003;24:1049-1056.

Tong KA, Ashwal S, Holshouser BA, et al. Hemorrhagic shearing lesions in children and adolescents with posttraumatic diffuse axonal injury: improved detection and initial results. Radiology. 2003;227:332-339.

Neuroradiology: THE REQUISITES, 2nd ed, pp 246, 256–258.

Comment

Diffuse axonal injury is the result of shear-strain forces induced by angular rotation or acceleration of the head that result in partial or complete disruption of involved axons. Patients have loss of consciousness and a spectrum of cognitive impairment and neurological dysfunction beginning at the moment of trauma. Symptoms may range from transient loss of consciousness at the time of injury to permanent coma (vegetative state) or death in the most severe diffuse forms. Diffuse axonal injury is most commonly seen in patients involved in high-velocity acceleration–deceleration motor vehicle accidents, but it can also be seen in more minor forms of trauma, such as a fall down stairs and occasionally falls from the standing position. It is characterized by multiple focal lesions in the lobar white matter at the gray–white matter interface, in the corpus callosum, and in cases of severe head trauma, in the dorsolateral brainstem. Shear injuries are typically elliptic in shape, with the long axis parallel to the direction of the involved axons.

Although MR imaging is the most sensitive imaging modality for the detection and evaluation of diffuse axonal injury, in the acute setting, the first radiologic study should be CT because the most critical issue is to detect potentially treatable acute intracranial hemorrhage (subdural and epidural hematomas, large parenchymal hematomas). If there is concern about shear injury, MR imaging should be performed when the patient is stable. Shear injuries, unless hemorrhagic or of substantial size, frequently go undetected on CT. The presence of intraventricular hemorrhage should raise suspicion of injury to the septum pellucidum or corpus callosum. On MR imaging, shear injuries are hyperintense on T2W images. Approximately 80% of shear injuries are nonhemorrhagic. In diffuse axonal injury associated with hemorrhage (as in this case), gradient echo susceptibility imaging shows blood products. In this case, the right thalamic and corpus callosal lesions are hypointense, consistent with the presence of blood products.

Notes

CASE 42 Glioblastoma Multiforme—Subependymal Spread

1. What is the primary imaging finding?

2. What is the differential diagnosis?

3. What is the best diagnosis in this case, and why?

4. In a patient with AIDS, what is the most likely cause of subependymal enhancement?

1. There is nodular enhancement along the subependyma of the left lateral ventricle (and a small amount along the right occipital horn).

CASE 42

2. Subependymal spread of neoplasm, including lymphoma, glioblastoma multiforme (GBM) [usually represents recurrent disease], and metastatic disease, such as breast and lung cancer. The inflammatory conditions that should be considered include sarcoid and tuberculosis. Although other infections can do this, the thick, nodular appearance in this case is more typical of neoplastic spread.

3. Recurrent subependymal GBM. The mild cerebral mass effect manifests as sulcal effacement in the left inferior frontal, temporal, and occipital lobes, consistent with infiltrating neoplasm. In addition, there is evidence of a previous craniotomy as well as an ill-defined parenchymal necrotic tumor extending to the left lateral ventricle seen on the second coronal image.

4. Lymphoma.

Christiforidis GA, Grecula JC, Newton HB, et al. Visualization of microvascularity in glioblastoma multiforme with 8-T high-spatial-resolution MR imaging. AJNR Am J Neuroradiol. 2002;23:1553-1556.

Neuroradiology: THE REQUISITES, 2nd ed, pp 128–129, 139, 142–143.

Comment

Glioblastoma multiforme classically presents with an ill-defined necrotic brain mass. The histologic grade of these aggressive neoplasms in adults progresses with age: the older the patient, the higher the histologic grade. Other imaging features that correlate with higher grades include enhancement, extensive mass effect, intratumoral necrosis, hemorrhage, vascularity and elevated relative cerebral blood volume, and elevated lactic acid on MR spectroscopy. Glioblastomas infiltrate the brain parenchyma, and this is manifest as T2W hyperintensity; however, there is little doubt that these neoplasms have also infiltrated into areas of the brain that appear normal on current diagnostic MR studies. Most GBMs enhance and usually demonstrate heterogeneity because of the presence of necrosis or hemorrhage. Enhancement may extend into the adjacent white matter. These tumors frequently cross the corpus callosum and the anterior or posterior commissures to spread to the contralateral cerebral hemisphere. Of the astrocytomas in adults, GBMs most commonly are associated with hemorrhage and subarachnoid seeding (2%–5%) of neoplasm. Occasionally, at presentation, GBMs will coat the subependyma or ependyma of the ventricles. However, it is important to recognize that although overall long-term survival rates in patients with GBM are still very poor, patients are living longer and in some instances with improved quality of life with changes in treatment protocols and in clinical trials looking at a spectrum of chemotherapeutic agents. Hence, in these patients, less typical patterns of disease progression on imaging, such as coating of the ventricles from subependymal tumor spread, will become more common, as in this case.

In a newly identified brain tumor in which biopsy is anticipated, regions of enhancement correlate with regions of solid tumor on pathology and have the best diagnostic yield. In addition, enhanced images may identify tumor spread to regions that otherwise would not be noticed on unenhanced images, such as the leptomeninges, subarachnoid space, or subependymal region along the ventricular margins, as in this case. In the postoperative setting, contrast may help to distinguish surgical change from residual tumor.

Notes

CASE 43 Amyloid Angiopathy

Walker DA, Broderick DF, Kotsenas AL, Rubino FA. Routine use of gradient-echo MRI to screen for cerebral amyloid angiopathy in elderly patients. Am J Roentgenol. 2004;182:1547-1550.

Neuroradiology: THE REQUISITES, 2nd ed, p 220.

Comment

Central nervous system amyloid angiopathy results from deposition of β-pleated proteins within the media and adventitia of small- and medium-sized vessels of the superficial layers of the cortex and leptomeninges. Amyloid deposition increases with age and results in loss of elasticity of the walls of involved vessels. On pathologic examination, microaneurysms and fibrinoid degeneration are often present. Amyloid stains intensely with Congo red dye (previously referred to as congophilic angiopathy) and demonstrates yellow-green birefringence under polarized light.

On CT and MR imaging, hemorrhages are characteristically lobar in location, and they most commonly occur in the frontal and parietal lobes. Multiple hemorrhages of different ages, as well as multiple simultaneous hemorrhages, are often present. Subarachnoid and subdural blood may be present due to perforation of blood through the pia arachnoid or involvement of superficial blood vessels with amyloid deposition. MR imaging, including gradient echo images, may be especially useful for demonstrating the full extent of intracranial involvement (CT readily shows acute hemorrhage, as in this case; however, regions of old blood products are often occult). Patients may have numerous small subcortical regions of focal hypointensity (multiple hypointense foci may also be related to cavernomas or microhemorrhages, as is seen in hypertension). Importantly, there is no association of hypertension with the development of amyloid angiopathy.

Notes

CASE 44 Mesial Temporal Sclerosis

Briellman RS, Syngeniotis A, Fleming S, et al. Increased anterior temporal lobe T2 times in cases of hippocampal sclerosis: a multi-echo T2 relaxometry study at 3T. Am J Neuroradiol. 2004;25:389-394.

Hogan RE, Wang L, Bertrand ME, et al. MRI-based high dimensional hippocampal mapping in mesial temporal lobe epilepsy. Brain. 2004;127:1731-1740.

Neuroradiology: THE REQUISITES, 2nd ed, pp 447–449.

Comment

Temporal lobe epilepsy is the most common epilepsy syndrome in adults. Seizures usually begin in late childhood or adolescence. Virtually all patients have complex partial seizures. In most patients, the epileptogenic focus involves the structures of the mesial temporal lobe. These structures include the hippocampus, amygdala, and parahippocampal gyrus. The histologic substrate in approximately two thirds of cases is mesial temporal sclerosis. The hippocampal formation located in the mesial temporal lobe protrudes into the medial temporal horn and is roofed by the choroidal fissure. It is a complex structure composed of the hippocampus proper, subiculum, dentate gyrus, parahippocampal gyrus, fimbria, and fornix. The hippocampus proper (or cornu ammonis) can be subdivided into four subfields, CA1 though CA4, depending on the appearance of pyramidal neurons. Neuronal loss is accompanied by fibrillary gliosis, leading to hippocampal atrophy. In mesial temporal sclerosis, gliosis may also affect the amygdala, uncus, and parahippocampal gyrus.

The differential diagnosis for hippocampal sclerosis includes cortical dysplasias and primary brain neoplasm. Mesial temporal sclerosis is usually radiologically characteristic. MR imaging using high-resolution thin-section coronal FLAIR and T2W and T1W gradient volumetric sequences is the imaging modality of choice for evaluating patients with seizure disorders. These cases illustrate the classic MR imaging appearance of hippocampal sclerosis in which there is atrophy of the left hippocampus in both cases as well as mild ipsilateral dilation of the adjacent temporal horn. Case A also shows T2W hyperintensity in the abnormal hippocampus that is believed to reflect gliosis.

Whether mesial temporal sclerosis is the cause or the result of temporal lobe epilepsy is controversial. Some studies have shown a relationship between complex infantile febrile seizures and mesial temporal sclerosis. Patients with complex febrile seizures (duration > 15 minutes, convulsive activity, or > 3 seizures within 24 hours) have an increased incidence of mesial temporal sclerosis.

Notes

CASE 45 Intraventricular Meningioma

Jelinek J, Smirniotopoulos JG, Parisi JE, Kanzer M. Lateral ventricular neoplasms of the brain: differential diagnosis based on clinical, CT, and MR findings. AJR Am J Roentgenol. 1990;155:365-372.

Majos C, Cucurella G, Aguilera C, Coll S, Pons LC. Intraventricular meningiomas: MR imaging and MR spectroscopic findings in two cases. AJNR Am J Neuroradiol. 1999;20:882-885.

Neuroradiology: THE REQUISITES, 2nd ed, p 101.

Comment

Cases A and B demonstrate well-demarcated mass lesions in the atria of the left lateral ventricle along the glomus of the choroid plexus, consistent with meningiomas. On T2W imaging, these tumors may range from mildly hyperintense to the brain parenchyma (however, markedly hypointense to CSF) to hypointense to brain tissue in cases of very cellular or calcified tumors. After contrast administration, there is homogeneous avid enhancement. In adults, this is the typical appearance of an intraventricular meningioma and the most common location for these neoplasms, which are speculated to arise from arachnoid rests within the choroid plexus. Like choroid plexus papillomas, intraventricular meningiomas occur slightly more often on the left, as illustrated in these cases. When large enough, intraventricular meningiomas may trap a particular segment of the lateral ventricle (usually the temporal or occipital horn), resulting in focal dilation and sometimes associated transependymal flow of CSF. When large enough, these tumors may compress the walls of the ventricles or grow through the ependyma, with resultant edema in the adjacent brain parenchyma. Their appearance on CT is similar to that of other intracranial meningiomas. On unenhanced CT images, these masses are often hyperdense with calcifications, as in Case B shown here. They avidly enhance after contrast administration.

The differential diagnosis of a mass in this location in adults includes glial neoplasms (astrocytomas, ependymomas), metastasis to the choroid plexus, and vascular lesions such as hemangiomas and cavernomas. Choroid plexus papillomas can usually be eliminated as a diagnostic consideration because they occur most commonly in children and because in adults they are usually located within the fourth ventricle.

Notes

CASE 46 Suprasellar Germinoma

Mah E, Rahmat K. Neurohypophyseal germinoma with metastasis to the spine. Eur J Radiol. 2007;63:89-92.

Neuroradiology: THE REQUISITES, 2nd ed, pp 550–552.

Comment

This case demonstrates a solid, avidly enhancing suprasellar mass that represented a germinoma. Due to their marked cellularity and protein content, germinomas are typically hyperdense on unenhanced CT and isointense to brain on T2W MR imaging. Cystic change and calcification are uncommon, and these neoplasms typically show prominent enhancement. On diffusion-weighted imaging, these may restrict being hyperintense, with corresponding low signal on apparent diffusion coefficient maps. These tumors can metastasize by subarachnoid seeding, and screening MR imaging of the spine should be performed.

Germinomas are most common in children and young adults, and they arise from primitive germ cells. The pineal gland is the most common site, followed by the suprasellar region. Clinical presentation from suprasellar masses is variable, but may include diabetes insipidus, hypopituitarism, or visual symptoms related to compression of the optic chiasm. Germinoma is the most common pineal tumor, accounting for 65% of all pineal germ cell neoplasms and approximately 40% of all pineal region tumors. Other germ cell tumors include teratoma, embryonal carcinoma, and choriocarcinoma. Teratomas may be distinguished from other germ cell tumors due to the presence of fat, calcification, and cyst formation (the fat and calcification or bone may have characteristic appearances on imaging). Choriocarcinomas may be differentiated due to the high incidence of hemorrhage within these tumors. In addition, β-human chorionic gonadotropin is a good serum marker for choriocarcinoma. Less common germ cell tumors, including embryonal cell carcinoma, endodermal sinus (yolk sac) tumors, and teratomas, may have hormonal markers such as β-human chorionic-gonadotropin and α-fetoprotein.

Notes

CASE 47 Mineral Deposition in the Basal Ganglia on T1W Imaging—Abnormal Calcium and Phosphate Metabolism

Baba Y, Ohkubo K, Hamada K, Hokotate H, Nakajo M. Hyperintense basal ganglia lesions on T1-weighted images in hereditary hemorrhagic telangiectasia with hepatic involvement. J Comput Assist Tomogr. 1998;22:976-979.

Komiyama M, Nakajima H, Nishikawa M, Yasui T. Chronological changes in nonhaemorrhagic brain infarcts with short T1 in the cerebellum and basal ganglia. Neuroradiology. 2000;42:492-498.

Neuroradiology: THE REQUISITES, 2nd ed, p 395.

Comment

This case illustrates bilaterally symmetric high signal intensity in the basal ganglia on unenhanced T1W images in a patient with chronic abnormalities in calcium and phosphate metabolism. It is important to note that the axial image is a gadolinium-enhanced study, and the bilaterally symmetric high signal intensity in the basal ganglia should not be mistaken for enhancement. High signal intensity in the basal ganglia on unenhanced T1W images is also described in patients with chronic liver failure, patients receiving hyperalimentation, and those with portosystemic shunting. The high signal intensity is believed to be most likely related to deposition of paramagnetic ions, particularly manganese; however, other materials, such as copper, have been suggested. In the setting of liver failure, high signal intensity is frequently most pronounced in the globus pallidus; however, it may also be noted in the putamen, brainstem, and pituitary gland.

Neurofibromatosis type 1 is the most common neurocutaneous disorder. It is associated with a variety of intracranial lesions, the most common of which are foci of high signal intensity on long TR images within the brain parenchyma. The foci of high signal intensity are seen most commonly in the basal ganglia; however, they are frequently noted in the white matter tracts of the corpus striatum, in the brainstem, and in the cerebellum. The basal ganglia lesions may be hyperintense on unenhanced T1W images. It has been suggested that the pathologic basis of these foci in neurofibromatosis type 1 may be related to hypomyelination, migrational abnormalities, and nonneoplastic hamartomatous changes. A recent study in which pathologic correlation was obtained suggests that at least some of the foci of signal abnormality may be related to vacuolar or spongiotic change.

Notes

CASE 48 Herpes Simplex Encephalitis—Type 1

Samann PG, Schlegel J, Muller G, Prantl F, Emminger C. Serial proton MR spectroscopy and diffusion imaging findings in HIV-related herpes simplex encephalitis. Am J Neuroradiol. 2003;24:2015-2019.

Neuroradiology: THE REQUISITES, 2nd ed, pp 288–290.

Comment

Type I herpes simplex virus produces necrotizing encephalitis in adults. The clinical presentation is varied, ranging from headache, fever, and seizures to coma. Radiologic evaluation frequently shows hypodensity with loss of gray–white matter differentiation in the temporal lobes and insular cortex on CT. Hemorrhage may also be present, as in this case. The CT appearance may simulate an infarct or a primary glial neoplasm. MR imaging findings in the acute stages of encephalitis show hyperintensity on long TR images within involved brain (usually the temporal lobes and inferomedial frontal lobes). There frequently is local mass effect, which is manifest by gyral expansion and sulcal effacement. Although bilateral disease is typical, herpes encephalitis usually involves the temporal lobes, insula, inferior frontal lobes, and cingulate gyrus in an asymmetric pattern. A proposed explanation for this pattern of involvement is the presence of the latent virus within the gasserian ganglion in Meckel’s cave. Reactivated virus may spread along the trigeminal nerve fibers, with subsequent spread along the meninges around the temporal lobes and the undersurface of the frontal lobes. Meningoencephalitis commonly results. Diagnosis may depend on brain biopsy with a positive viral culture or identification of viral inclusion bodies. A positive result on herpes simplex virus polymerase chain reaction testing is diagnostic, and results of this test are available before those from cultures. Cortical gyriform enhancement is often present and may be associated with meningeal enhancement.

A good outcome from herpes simplex encephalitis relies on early diagnosis, which is of course dependent on considering herpes as a diagnosis! Delay in therapy (acyclovir) or untreated herpes is associated with a high mortality rate (50%–75%), with little chance of a full neurologic recovery.

Notes

CASE 49 Primary Orbital Lymphoma

Holland D, Muane S, Kovacs G, Behrendt S. Metastatic tumors of the orbit: a retrospective study. Orbit. 2003;22:15-24.

Shields JA, Shields CL, Brotman HK, et al. Cancer metastatic to the orbit. Ophthal Plast Reconstr Surg. 2001;17:346-354.

Neuroradiology: THE REQUISITES, 2nd ed, pp 501, 503.

Comment

Clinical manifestations of ocular metastases and lymphoma are variable, depending on the site of involvement, ranging from asymptomatic to proptosis, diplopia, decreased vision, and less commonly, pain, red eye, and lid swelling. The symptoms of orbital metastasis may precede detection of the primary tumor in up to 25% of cases. In autopsy series, up to 7% of patients with known systemic carcinoma have metastases to the orbit. The presence of orbital metastases is an unfavorable prognostic sign, with an average mean survival time of less than 2 years. Management is palliative and may include radiation, chemotherapy, or surgery, and is intended to preserve vision, provide symptomatic relief, and improve quality of life.

The most common location of orbital metastases is to the globe. Ocular metastases characteristically involve the uveal region, resulting in thickening in this location on imaging. Intraconal retrobulbar disease is usually related to direct extension of an ocular metastasis. In most cases, metastasis occurs through hematogenous spread. The most common tumors to metastasize to the globe are breast, followed by prostate carcinoma in adults. Outside of the globe, orbital metastases most often are extraconal and are usually related to bone metastases (prostate carcinoma is most common). Extraosseous spread from a bone metastasis frequently invades the adjacent extraocular muscle.

Lymphoma of the orbit can be unilateral or bilateral and simultaneous and part of systemic disease, or can be isolated (primary) to the orbit. Primary orbital lymphomas histologically are usually low grade (60%) B-cell types. Primary lymphoma involves the eyelid and extraocular muscles in the majority of cases (up to 40%), the conjunctiva in 33% of cases, and the lacrimal apparatus in 25% of cases. These lesions are usually managed with radiation therapy, and some higher-grade lesions also receive chemotherapy. Distant recurrences are reported in approximately 15% of cases.

Notes

CASE 50 Basilar Meningitis and Encephalitis—Tuberculosis

1. What are the imaging findings?

2. What disease processes affect the basilar meninges?

3. Is hydrocephalus associated with meningitis typically communicating or noncommunicating?

4. What primary CNS neoplasms have a predilection for subarachnoid seeding?

1. Diffuse enhancement of the basal cisterns, T2W hyperintensity in the midbrain, and a ring-enhancing lesion in the medial left temporal lobe.

CASE 50

2. Infection (eg, tuberculosis, neurosyphilis, pyogenic infections, Cryptococcus), sarcoid, leptomeningeal seeding of tumor (carcinomatous from systemic malignancies or primary brain tumors), lymphoma, and chemical meningitides (eg, drugs, iodophenylundecylic acid [Pantopaque], fat from ruptured dermoids).

3. The hydrocephalus is usually communicating due to blockage of the basal cisterns and arachnoid villi with an inflammatory exudate. Hydrocephalus may also result from mass effect related to a parenchymal lesion, or from entrapment of a ventricle related to ependymitis.

4. Primitive neuroectodermal tumors (medulloblastoma, pineoblastoma), germinoma, glial neoplasms (glioblastoma multiforme, oligodendroglioma), and choroid plexus papilloma.

Bernaerts A, Vanhoenacker FM, Parizel PM, et al. Tuberculosis of the central nervous system: overview of neuroradiological findings. Eur Radiol. 2003;13:1876-1890.

Gupta RK, Vatsal DK, Husain N, Chawla S, Prasad KN, Roy R. Differentiation of tuberculous from pyogenic brain abscesses with in vivo proton MR spectroscopy and magnetization transfer MR imaging. AJNR Am J Neuroradiol. 2001;22:1503-1509.