Radiology Case Vignettes Kapisoor Singh, Karunakaran M, Jai Vinod Shah
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NeuroimagingChapter 1

 
CASE-1
A 58-year-old male with acute onset seizures and raised blood pressure.
zoom view
Figs 1.1A to D:
 
Diagnosis
  • Acute hypertensive encephalopathy
  • Posterior reversible encephalopathy syndrome
  • Reversible posterior leukoencephalopathy syndrome.
2
 
Findings
Bi-occipito-parietal foci of increased T2 signal intensities involving the cortex and subcortical white matter on fluid attenuated inversion recovery (FLAIR) (A and B) and diffusion weighted imaging (DWI) (C) with increased apparent diffusion coefficient (ADC) values (D).
 
Discussion
Acute hypertensive encephalopathy [also called posterior reversible encephalopathy syndrome (PRES)] is a disorder of cerebral vascular autoregulation with multiple etiologies, most of which cause acute/subacute hypertension (acute systemic hypertension, pre-eclampsia, eclampsia, uremic encephalopathy, drug toxicity).
The predilection for involvement of posterior circulation territories is generally accepted to be resulting from the relatively sparse sympathetic innervation (poor autoregulation) of the vertebrobasilar circulation leading to damage of vascular endothelium in acute hypertension and breech of blood–brain barrier.
Magnetic resonance imaging (MRI) with diffusion-weighted sequences provides a powerful means of diagnosing PRES. The hallmark of this diagnosis is vasogenic edema in the territories of the posterior circulation, which can be reliably differentiated from cytotoxic edema in other etiologies by using DWI and by calculating the ADC map, which in the early phase shows elevated ADC values. Involvement of anterior circulation structures is also common and should not deter consideration of this diagnosis.
In late phases, diffusion-weighted images may show foci of high signal intensity in cortex that is either undergoing infarction or at high risk of infarction. ADC values in these areas first become normal (pseudonormalization) and this finding may represent an early sign of non-reversibility in PRES, heralding the conversion to infarction when the ADC values are reduced (restricted diffusion). Intracranial hemorrhage (DWI shows heterogeneous signal intensities) and brain stem involvement are associated with a poor prognosis.
 
Differential Diagnosis
  • Acute cerebral ischemia
  • Acute cerebral hyperemia (postictal, recent decompression of chronic SDH, post carotid endarterectomy/angioplasty)
  • Metabolic derangements like dialysis disequilibrium syndrome, porphyria
  • Posterior circulation infarcts.
  • Cyclosporine toxicity.
3
 
CASE-2
A 4-year-old girl with headache, nausea and vomiting.
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Figs 1.2A to D: (A) T1 contrast; (B) T1WI; (C) T2WI; (D) MR sepectroscopy
 
Findings
Intraventricular mass in fourth ventricle causing obstructive hydrocephalus, compression of brainstem and cerebellar tonsillar herniation, showing heterogeneous hyperintense T2W signals and heterogeneous iso- to hypointense T1WI signals with heterogeneous contrast uptake and few calcifications within. On magnetic resonance spectroscopy, increased myoinositol 3.6 ppm; most prominent peak, increased lipids 0.9 and 1.3 ppm, increased Glx glutamine and glutamate at 2.1 to 2.5 ppm and reduced N-acetyl aspartate 2.0 ppm peaks noted; Taurine 3.3 ppm and guanine 3.8 ppm are not significant which are often seen in primitive neuroectodermal tumor (PNET) medulloblastoma (MB)/germinoma.
 
Diagnosis
  • Ependymoma.
4
 
Discussion
Ependymomas make up 8–10% of all primary intracranial tumors in children and 15% of all infratentorial tumors. They are more frequently infratentorial 70%, and in 30% of cases, supratentorial.
Infratentorial ependymomas originate from ependymal cells lining the fourth ventricle. The tumor expands through the foramen of Magendie, into cisterna magna and even into the superior part of the vertebral canal. Spinal ependymomas are associated with neurofibromatosis, type-2 (NF2).
On routine computed tomography (CT), ependymoma is isodense relative to brain tissue. Formation of cysts is seen in 20% of cases. Small calcifications are seen in 50% of cases, which makes ependymomas the most frequent type of infratentorial tumors with calcifications. Contrast enhancement on CT is moderate.
On MRI, typical ependymomas appear as heterogeneous masses, completely occupying the cavity of the fourth ventricle and expand into the cisterna magna or the lateral pontine cistern. The solid part of ependymomas appears hypointense on T1-weighted images (T1WI) and hyperintense on T2-weighted images (T2WI). Cysts give more hyperintense signal than that of the cerebrospinal fluid (CSF) on T1WI and look brighter on T2WI relative to tumor tissue. The signal heterogeneity of the tumor stroma is due to cysts, microcalcifications, foci with newly formed vessels, and less often, microhemorrhages. Benign ependymomas show moderate and heterogeneous contrast enhancement. If a tumor is large and occludes the fourth ventricle and foramen of Magendie, then hydrocephalus often develops. Malignant ependymomas are more heterogeneous and produce more prominent contrast enhancement.
 
Differential Diagnosis
  • Primitive neuroectodermal tumor/medulloblastoma
  • Atypical teratoid/rhabdoid tumor.
5
 
CASE-3
A 82-year-old male with severe headache and giddiness since one year.
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Figs 1.3A to D: (A) T2WI; (B) T1WI; (C) T1contrast; (D) DWI
 
Findings
Right cerebellopontine angle extra-axial mass extending into internal auditory meatus and compressing adjacent brainstem—‘ice-cream cone’ appearance. The mass lesion shows heterogeneous hypointense signal on T1W (A), hyperintense signals on T2W (B) and T2-FLAIR (C), and DWI (D). Another extra-axial cystic lesion posterior to the mass showing CSF like signals on all sequences.
 
Diagnosis
  • Schwannoma with arachnoid cyst.
6
 
Discussion
The rubric ‘peripheral nerve sheath tumor’ actually defines several unique pathologic entities including schwannoma, neurofibroma, perineurioma, traumatic neuroma (non-neoplastic; all benign), and malignant peripheral nerve sheath tumor.
Schwannomas are derived from the myelinating cell of the peripheral nervous system and are composed almost entirely of Schwann cells. By contrast, neurofibromas appear to contain all the cellular elements of a peripheral nerve, including Schwann cells, fibroblasts, perineurial cells, and axons. The tumor cells grow diffusely within and along nerves, causing the nerves to expand radially while entrapping native neural elements within the substance of the tumor. This intraneural growth pattern, with its entrapped axons, provides a key feature to histologically distinguish neurofibroma from schwannoma.
The eighth cranial nerve sheath tumor is usually a schwannoma originating from the vestibular portion of the nerve. According to location the following three categories of eighth nerve neurinomas are distinguished: Intrachannel located within porus acusticus internus; Intra- and extrachannel: They expand into porus acusticus internus as well as into the cerebellopontine cistern; Extrachannel: They originate from the intradural nerve portion that passes through the cerebellopontine cistern. Vestibular schwannomas rarely undergo malignant transformation.
On CT, schwannomas <1 cm in size are not easily identified. Most of them dilate the meatus acusticus internus. They show marked contrast enhancement. On MRI, they are iso- to hypointense on T1WI and heterogeneously hyperintense on T2WI with some cystic degeneration.
 
Differential Diagnosis
  • Meningioma
  • Ependymoma
  • Choroid plexus papilloma
7
 
CASE-4
A 3-year-old girl with headache and vomiting since 1 month.
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Figs 1.4A to D:
 
Findings
Predominantly solid lesion involving roof and floor of fourth ventricle, right half of pons and medulla and right middle cerebellar peduncle with heterogeneous contrast enhancement causing IV ventricular obliteration and obstructive dilatation of lateral and third ventricles. The lesion appears hyperdense on CT (A), iso- to hypointense on T1W (B) and T2W (D) with heterogeneous contrast enhancement on contrast-enhanced magnetic resonance imaging (C) with a peripheral cystic component.
 
Diagnosis
  • Medulloblastoma.
 
Discussion
Medulloblastoma is a primitive neuroectodermal tumor originating from inferior medullary velum/roof of the 4th ventricle. PNETs include medulloblastomas, medulloepitheliomas, pigmented medulloblastomas,8 ependymoblastomas, pineoblastomas, and cerebral neuroblastomas. These tumors originate from undifferentiated cells in the subependymal region in the fetal brain. PNETs are second to the cerebellar astrocytoma in frequency, comprising 25% of intracranial tumors in children. Peak age is 2–8 years.
Symptoms are caused by compression of the CSF pathways and obstructive hydrocephalus. Radiographic features includes midline hyperdense cerebellar mass showing typically intense and homogenous enhancement. The mass shows intermediate signal intensity on T2W with/without hydrocephalus and calcifications. Rapid growth occurs into cerebellar hemisphere, brainstem, and spine. CSF seeding to spinal cord (‘drop metastasis’) and meninges occurs. Systemic metastases can occur and appear as sclerotic lesions in bone. Metastases to abdominal cavity may occur via a VP shunt.
They are highly radiosensitive but metastasize early via CSF. They have association some with certain syndromes such as Gorlin's syndrome (basal cell nevi, odontogenic keratocysts, falx calcification) or Turcot's syndrome (colonic polyps and central nervous system (CNS) malignancy).
 
Differential Diagnosis
  • Ependymoma
  • Choroid plexus papilloma
  • Brainstem glioma.
9
 
CASE-5
A 49-year-old female with chronic headache.
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Figs 1.5A to D: (A) T1WI; (B) T2WI; (C) FLAIR; (D) T1 contrast
 
Findings
Axial T1W (A); axial T2W (B and C) and sagittal contrast enhanced T1W (D) MR images reveals a well-defined heterogeneous expansile destructive lesion in the right greater wing of sphenoid with impingement upon orbital cone and the optic nerve and from a posterolateral direction, destruction of adjacent floor of middle cranial fossa, including foramen rotundum and lateral vidian canal wall. The lesion extends into right sphenoid sinus as well as intra- cranially into adjacent right temporal cerebrum with multiple cystic areas within. The skull base lesion exhibits heterogeneous contrast enhancement.
 
Diagnosis
  • Chondrosarcoma.
10
 
Discussion
Chondrosarcomas can arise from bone, cartilage, or even tissues without a cartilaginous component, and 6.5% of these tumors arise in the head and neck region. These tumors have a particular propensity for the petro-occipital (petroclival) synchondrosis or fissure, and thus chondroid tumors in the deep skull base region tend to be off midline. Chondrosarcoma invades locally but seldom metastasizes. Tumors spread away from the petro-occipital fissure, involve the clivus and petrous portion of the temporal bone, and bulge into the subarachnoid space cisterns or into the soft tissues beneath the skull base. Conventional chondrosarcomas can be graded, reflecting degrees of differentiation. Almost all chondrosarcomas of the central skull base are well or moderately differentiated. Most are slow growing. Chondrosarcomas can occur at almost any age, but most occur in middle age. The presentation depends on the location and local extension.
On CT, chondrosarcomas have a varied appearance, depending on the amount of chondroid matrix present. There is usually a significant soft-tissue component that has a dense appearance on noncontrast studies and enhances to some degree after contrast administration. Calcification of the tumor matrix is characteristic but is not always present. The calcifications tend to be small ringlets or incomplete rings,
On MRI, these tumors usually have an intermediate T1-weighted and a fairly high T2-weighted signal intensity. After gadolinium administration there is detectable enhancement, but not profound.
Chondrosarcoma can occur in Ollier's disease (multiple enchondromatosis) and Maffucci syndrome (multiple enchondromas with associated cutaneous hemangiomas). Chondrosarcoma can also complicate Paget's disease.
 
Differential Diagnosis
  • Chordoma
  • Chondroblastoma.
11
 
CASE-6
A 6-month-old baby with delayed mile stones and focal seizures.
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Figs 1.6A to D: (A) Plain CT; (B) Contrast CT; (C) Plain CT; (D) Contrast CT
 
Findings
Computed tomography scan of brain (plain and contrast) reveals marked atrophy of right frontal lobe, widening of subarachnoid spaces and ipsilateral prominent choroids plexus, periventricular venules and subependymal veins.
 
Diagnosis
  • Sturge-Weber-Dimitri syndrome
  • Encephalotrigeminal angiomatosis.
 
Discussion
Sturge-Weber syndrome (SWS) is a congenital disorder caused by the persistence of the transitory primordial sinusoidal plexus stage of vessel12 development. SWS is usually sporadic and characterized by a vascular malformation, with capillary and/or venous malformation that involve the face, choroid of the eye, and leptomeninges. The facial vascular malformation has a predilection for the distribution of the first division of the trigeminal nerve. The disease process is usually unilateral.
Plain skull radiographs may show ipsilateral skull-table and orbital thickening, elevation of the sphenoid wing and petrous ridge, and enlarged ipsilateral paranasal sinuses and mastoid air cells due to underlying ipsilateral cerebral atrophy. Plain radiographs of the skull in older children and adults may reveal asymmetry, with a smaller hemicranium and gyriform intracranial calcification on the ipsilateral side.
Computed tomography scans show the tramline gyriform calcification of opposing gyri that underlies the contrast-enhancing leptomeningeal vascular malformation. The subjacent white matter may be hypoattenuating on CT scans. The ipsilateral choroid plexus may be enlarged. Enlarged transcortical (medullary) veins are frequently associated with an enlarged choroid glomus. Other features on CT scans include ipsilateral cortical atrophy, enlargement of the ipsilateral ventricle, and loss of volume of the ipsilateral cranial cavity.
Magnetic resonance imaging reveals a pial, enhancing, angiomatous malformation, often in the occipital or posterior temporoparietal region ipsilateral to the facial angioma. MRI demonstrates atrophy of the cerebral hemisphere subjacent to the leptomeningeal angioma, with small gyri and enlarged adjacent sulci. Although MRI is not as good as CT in depicting calcification, it is superior to CT in the demonstration of abnormal myelination. Cerebral angiograms show early capillary blush in the areas involved with the pial vascular malformation associated with abnormally large veins in the subependymal and periventricular regions. Enlarged deep medullary veins that drain deep to the subependymal veins are present.
 
Differential Diagnosis
  • Tuberous sclerosis
  • Klippel-Trenaunay syndrome
  • Wyburn-Mason syndrome.13
 
CASE-7
History of progressive loss of vision.
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Figs 1.7A to D:
 
Findings
Axial FLAIR (A), contrast enhanced T1W (B), gradient echo (C) and coronal T2W (D) MR images reveal a large extra-axial sellar and suprasellar mass lesion indenting the right basal ganglia/thalamus and frontal lobe, right cavernous sinus, optic chiasm and midbrain and cousin a subfalcine herniation to the left. The mass appears hyperintense on T2-FLAIR, hypointense on T2W and shows contrast enhancement.
 
Diagnosis
  • Hemorrhagic pituitary macroadenoma.
 
Discussion
Pituitary adenomas rank third commonest among tumors of the CNS and make up 4–17% of all brain tumors. The peak incidence is between 20 and14 40 years. Usually they are classified according to their size: less than 10 mm (microadenomas), greater than 10 mm (macroadenomas).
  • Kadashev et al. have subdivided adenomas as follows: According to size
  • Normal sella turcica, small (16–25 mm); intermediate (26–35 mm); large (36–59 mm); giant (>60 mm): According to the direction of growth
  • Infrasellar into the sphenoidal sinus or nasopharynx
  • Antesellar towards the platform of the sphenoid bone, into the ethmoid labyrinth
  • Retrosellar behind the dorsum sellae, onto clivus, with destruction of the dorsum sellae, or passing by and onto the clivus, beneath dura mater
  • Laterosellar into the cavernous sinus or under duramater of the middle cranial fossa
  • Suprasellar region above sella.
Hormonally inactive adenomas usually reach large size by the time of clinical signs appear. They expand upwards into the suprasellar cistern, laterally into cavernous sinuses, or downwards into the sphenoidal sinus.
Compression of optic nerves causes vision impairment. The continued upward growth causes compression of the third ventricle and occlusion of the foramina of Monro, which contributes to obstructive hydrocephalus.
Expansion into cavernous sinuses causes compression of cranial nerves that pass there, which may lead to diplopia and anesthesia of the face. Compression of the rest of the pituitary gland mainly causes anterior lobe dysfunction. Involvement of neurohypophysis and the pituitary stalk may cause diabetes insipidus.
In rare cases, the pituitary adenoma may be manifested by the infarction of the pituitary gland due to intratumoral hemorrhage. Subacute hemorrhage shows hyperintense signal on both T1W and T2W images.
Malignant tumors are characterized by rapid growth, frequent hemorrhages, and extended invasion of the surrounding structures.
 
Differential Diagnosis
  • Suprasellar meningioma.15
 
CASE-8
A 3-year-old baby with seizures.
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Figs 1.8A to D:
 
Findings
Axial and sagittal T1W (A and B) and coronal T2W (C and D) MR images reveal absent corpus callosum, high riding third ventricle, parallel lateral ventricles, longitudinal bundles of white matter medial to the lateral ventricles with colpocephaly.
 
Diagnosis
  • Agenesis of corpus callosum.
 
Discussion
Agenesis of the corpus callosum (ACC) has a prevalence of 0.3% in the general population. The corpus callosum develops from the lamina reuniens in the telencephalon; it begins to appear between the anterior and hippocampal commissures at about 10.5 weeks. The adult form of the corpus callosum is achieved by 17 weeks’ gestational age. Initial formation of the corpus callosum occurs in the genu and the body, progressing posteriorly. The anterior genu and rostrum develop last, folding back under the genu. The callosum thickens with increasing myelination. Callosal agenesis is believed16 to be caused by a vascular or inflammatory lesion that develops before 12 weeks of gestation (i.e. before its complete development).
In complete agenesis, the corpus callosum is totally absent. In partial agenesis (hypoplasia), the anterior portion (posterior genu and anterior body) is formed, but the posterior portion (posterior body and splenium) is not formed. The rostrum and the anterior genu are also not formed.
When the corpus callosum is absent, the third ventricle is often high riding, extending superiorly between the lateral ventricles. On axial imaging, the lateral ventricles are parallel. Medial to the lateral ventricles, longitudinal bundles (Probst bundles) of white matter are present in ACC. The occipital horns of the lateral ventricles are dilated probably because of a deficiency of peritrigonal white-matter fibers. This anatomic finding is known as colpocephaly. When the corpus callosum is absent, the cingulate gyrus is inverted, the normal cingulate sulcus is absent, and the medial cerebral sulci radiate toward the midline in a radial configuration. The hippocampal formations are frequently hypoplastic in patients with ACC, with resulting mild dilatation of the temporal horns.
Antenatal diagnosis of ACC is possible from about 20 weeks’ gestation. MRI permits confident diagnosis of ACC and its associated anomalies. MRI shows the anatomic features of ACC better than CT does.
 
Differential Diagnosis
  • Holoprosencephaly
  • Aicardi syndrome
  • Apert syndrome.17
 
CASE-9
History of headache, vomiting since two weeks.
zoom view
Figs 1.9A to D:
 
Findings
Coronal T2W (A), contrast enhanced T1W sagittal (B) and axial (C and D) MR images reveal a large heterogeneously enhancing complex mass lesion with a cystic component and areas of hemorrhagic foci within cyst, in the hypothalamic region extending into prepontine/premedullary cisterns. The mass is extending into the third ventricle, compressing and posteriorly displacing the brainstem, fourth ventricle and cerebellum, causing dilatation of the third and lateral ventricles.
 
Diagnosis
  • Pilocytic astrocytoma.
 
Discussion
Pilocytic astrocytoma is the most common pediatric CNS glial neoplasm and the most common pediatric cerebellar tumor. This tumor has benign18 biologic behavior with high survival rate—94% at 10 years. It typically occurs in cerebellum (60%), optic nerve and chiasm (25–30%), and hypothalamic region. Classic appearance is a cystic mass with an enhancing mural nodule. Less common appearances are quite nonspecific. Surrounding vasogenic edema is rarely present.
Obstructive hydrocephalus occurs late (usually mild to moderate), and 10% of pilocytic astrocytoma have calcification. It has an association with neurofibromatosis type-1 (15–21%) and typical involves optic nerve/chiasm.
Computed tomography appearance: Hypodense cyst like component combined with isodense soft-tissue mural nodule.
Magnetic resonance imaging appearance: On T1WI, intense to hypointense; on T2WI, hyperintense (cystic portion), mixed signal (soft-tissue portion); mural nodule shows intense enhancement. Other patterns: ringlike enhancement of cysts, solid near homogeneous enhancement, necrosis with central nonenhancing zone. Leptomeningeal metastases are rare.
 
Differential Diagnosis
  • Medulloblastoma
  • Ependymoma
  • Pilomyxoid astrocytoma
  • Atypical teratoid-rhabdoid tumor
  • Hemangioblastoma.19
 
CASE-10
Patient with head trauma.
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Figs 1.10A to D:
 
Findings
Axial images (A and B) show hemorrhagic contusion in bilateral temporal cerebrum and left temporal subdural hemorrhage. Axial image (C) reveals a large right frontal extradural hemorrhage with midline shift to the left. VRT (D) image reveals fracture of the frontal bone. Fracture line is crossing the superior sagittal sinus.
 
Diagnosis
  • Cranial fracture, large frontal extradural hematoma causing leftward shift of anterior midline, with bilateral temporal cerebral contusions.
 
Discussion
  • Plain CT scanning is usually the first evaluation in patients with head trauma providing a quick assessment of brain contusions, subdural and20 extradural hematomas and ensuing mass effects/brain herniations, as well as craniofacial fractures. Contrast CT or CT cerebral angiography can be performed if major vascular/venous sinus injury or thrombosis is suspected. Small hemorrhages particularly brainstem contusions may be missed on CT scans. Microhemorrhages in diffuse axonal injury may be missed sometimes and the CT may appear normal/near-normal in spite of profound alteration in mental status of the patient.21
 
CASE-11
A 35-year-old male with spastic right hemiparesis and developmental delay sustained minor head trauma.
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Figs 1.11A to D:
 
Findings
Axial CT images brain window (A and B) and bone window (C and D) reveal no significant acute traumatic brain injury but unrelated finding of cystic encephalomalacic changes in left perisylvian cerebrum (MCA territory) and ex vacuo dilatation of left lateral ventricle. The ischemic insult was likely sustained in utero (2nd trimester) and resulting left cerebral atrophy has resulted in reduced developmental expansion and thickening of overlying cranial vault with compensatory over-development of left frontal sinus.
 
Diagnosis
  • Dyke-Davidoff-Masson syndrome.22
 
Discussion
Dyke-Davidoff-Masson syndrome refers to atrophy or hypoplasia of one cerebral hemisphere (hemiatrophy) which is secondary to brain insult in fetal or early childhood period.
In the primary (congenital) type, the entire cerebral hemisphere is characteristically hypoplastic. The secondary type results from a cerebrovascular lesion, inflammatory process, or cranial trauma. The brain reaches half of its adult size during the first year of life and reaches three-fourths of that size by the end of third year. As it enlarges, the brain presses outward on the bony tables and is partly responsible for the gradual enlargement and general shape of the adult head. When the brain fails to grow properly, the other structures tend to direct their growth inward, thus accounting for the enlargement of the frontal sinus, the increased width of the diploic space and the elevations of the greater wing of sphenoid and the petrous ridge on the affected side. These changes can occur only when brain damage is sustained before three years of age however, such changes may become evident as soon as nine-months after brain damage was sustained.
A vascular cause of cerebral hemiatrophy (hypoplasia): It was proposed that a vascular anomaly occurring in very early gestation (five or six weeks) may result in a major defect in brain development whereas those occurring later may produce more localized lesions. The plain skull radiographic changes include thickening of calvarium and dilatation of ipsilateral frontal and ethmoid sinuses. Also, there is elevation of the greater wing of sphenoid and petrous ridge and upward tilting of planum-sphenoidale.
 
Differential Diagnosis
  • Sturge-Weber syndrome
  • Silver syndrome
  • Linear nevus syndrome.23
 
CASE-12
A 64-year-old disoriented male with frequent headaches.
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Figs 1.12A to D:
 
Findings
Axial T2-FLAIR (A) and T2W (B); sagittal T1W (C); coronal T2W (D) images reveal heterogeneous complex mass lesion with cystic components arising from the genu and body of corpus callosum, infiltrating adjacent superior surfaces of both lateral ventricles with perilesional white matter edema. The lesion showed heterogeneous contrast enhancement (images not shown).
 
Diagnosis
  • Corpus callosum glioma (high-grade/glioblastoma multiforme).
 
Discussion
Glioblastoma multiforme (GBM) is an extremely aggressive diffuse astrocytic tumor commonly found in the supratentorial white matter of the cerebral24 hemispheres. It is the most common primary brain tumor in adults, accounting for 25% of all cases. Glioblastomas most commonly spread via direct extension along white matter tracts, including the corpus callosum, although hematogenous, subependymal, and CSF spread can also be seen. When the corpus callosum is affected, GBM commonly display a characteristic bihemispheric involvement, resulting in a classic butterfly pattern. On MRI, these tumors typically enhance solidly and intensely in the corpus callosum, although occasionally no enhancement is seen. Because the corpus callosum is relatively resistant to infiltration, GBM should be considered for any lesion crossing the corpus callosum.
 
Differential Diagnosis
  • Primary CNS lymphoma (AIDS/immunocompromised patient)
  • Tumefactive demyelination
  • Metastasis.
25
 
CASE-13
Patient came with headache since one week and altered sensorium.
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Figs 1.13A to D:
 
Findings
Axial T1W (A); T2W (B); coronal T2W (C) and contrast enhanced T1W (D) images reveals heterogeneously enhancing lesion in the right temporoparietal region with exuberant perilesional edema with mass effect causing midline shift and subfalcine herniation to the left.
 
Diagnosis
  • Glioblastoma multiforme.
 
Discussion
Glioblastomas (malignant glioma) are the most common adult malignant brain tumors, and 20% of all primary brain neoplasms are GBM tumors.
Glioblastoma multiforme is the highest-grade form of astrocytoma and makes up about two thirds of all brain astrocytomas, as well as 20% of primary brain neoplasms. Glioblastomas are the most common adult malignant brain tumors. The peak age for the GBM diagnosis is 50–70 years.26
Although computed tomography can demonstrate the tumor and associated findings, the modality of choice for the examination of a patient with suspected or confirmed GBM is MRI. Positron emission tomography is useful after surgical resection to differentiate between recurrent tumor and scar tissue.
In terms of the imaging appearance and the appearance of a mass in the spectrum from low-grade astrocytoma to GBM, some generalizations can be made. The incidence of calcification decreases in the spectrum from low-grade astrocytoma to GBM. The incidence of enhancement increases in the spectrum from low-grade astrocytoma [preserved blood–brain barrier (BBB), low enhancement frequency] to GBM (disrupted BBB). Hemorrhage, necrosis, mass effect, and edema incidence patterns are the same as those for enhancement. Unless hemorrhagic changes are present, most tumors are hypointense on T1W MRI scan and hyperintense on T2W MRI. Enhancement on CT scans means enhancement on MRI scan.
 
Differential Diagnosis
  • Anaplastic astrocytoma
  • Metastasis
  • Arteriovenous malformation with hemorrhage
  • Gliosarcoma
  • Malignant meningioma
  • Hemangiopericytoma.27
 
CASE-14
A 22-year-old female with high fever, headache, vomiting and seizures.
zoom view
Figs 1.14A and B:
 
Findings
Axial (A) CT of brain reveals multiple coalescent heterogeneously and peripherally enhancing lesions in the left lobe of cerebellum. Coronal (B) CT of thorax reveals bilateral upper lobe fibrosis (L>R) with volume loss on the left and raised left hemidiaphragm.
 
Diagnosis
  • Tuberculoma.
 
Discussion
Involvement of the central nervous system occurs in 5 percent of cases of tuberculosis, and is especially common in patients younger than 20 years. Signs of neurotuberculosis are miscellaneous, ranging from a diffuse form—TB leptomeningitis—to focal forms, such as cerebritis/abscess and tuberculoma.
Mycobacteria enter meninges and superficial brain tissue via a hematogenic route from lungs. Here microbes remain inactive in the tubercles or microgranulomas (Rich's foci), which later may rupture into the subarachnoid space and cause tuberculosis of meninges.
Computed tomography shows obliteration of the basal cisterns by isodense or slightly hyperdense exudate, which shows diffuse enhancement with IV contrast medium.28
The most useful CT criteria of abnormal basal meningeal enhancement are: (A) linear enhancement of the middle cerebral artery cisterns; (B) obliteration by contrast of the CSF spaces around normal vascular enhancement; (C) Y-shaped enhancement at the junction of the suprasellar and middle cerebral artery cisterns and (D) asymmetry of enhancement.
The meningeal exudate obstructs CSF resorption and causes communicating hydrocephalus; this is seen in 50 percent of adults and 85 percent of children. MRI depicts the basal meningeal enhancement, hydrocephalus and basal ganglia infarcts with greater sensitivity than CT.
Tuberculomas (parenchymal granulomas) occur most often at the corticomedullary junction. On CT they appear as small, rounded lesions isodense or hypodense to brain, with variable amounts of surrounding edema. Enhancement is homogeneous when lesions are solid and shows rim enhancement when central caseation or liquefaction occurs.
 
Differential Diagnosis
  • Infectious cerebellitis (bacterial, fungal, viral, parasitic)
  • Glioblastoma multiforme
  • Neurosarcoidosis.
29
 
CASE-15
A 17-year-old female with seizures
zoom view
Figs 1.15A to C:
 
Findings
Axial plain CT images revealed broad gyri, thickened grey matter and shallow sulci in both frontal cerebral lobes.
 
Diagnosis
  • Pachygyria.
 
Discussion
  • Pachygyria means presence of wide and flat gyri and is synonymous with incomplete lissencephaly. Focal area of loss of sulci and gyri with thickening of cortical gray matter differentiates from tumor. Typically located in the frontoparietal regions.
  • On nonenhanced computed tomography, thick, smooth cortex with shallow sulci, flat gyri; Cobblestone pebbled cortex (Neurons over migrate through gaps in external layer of cortex creating a pebbled contour of the brain surface) with other brain malformations.30
  • On TlWI and T2WI, incomplete lissencephaly, vertical shallow sylvian fissures, smooth brain with thick cortex and thin outer gray matter mantle, irregular cortical projections into white matter, and hypomyelination are common. Ocular and cerebral anomalies and hydrocephalus secondary to aqueductal stenosis may be associated.31
 
CASE-16
Known case of sinonasal polyposis, post-polypectomy and sinus surgery. Presented with headache and vomiting.
zoom view
Figs 1.16A to D:
 
Findings
Axial contrast enhanced T1W (A), T2-FLAIR (B), T2W (C); coronal T2W (D) images reveal a thick-rim enhancing lesion in the right frontal lobe with perilesional edema, dilated ventricles, enhancing ventricular ependyma.
 
Diagnosis
  • Frontal abscess with hydrocephalus and ventriculitis.
 
Discussion
Intracranial abscesses can originate from infection of contiguous structures (e.g. otitis media, dental infection, mastoiditis, sinusitis) secondary to32 hematogenous spread from a remote site (especially in patients with cyanotic congenital heart disease), after skull trauma or surgery, and, rarely, following meningitis. Contiguous suppurative focus is seen in 45–50% of cases.
Direct extension may occur through necrotic areas of osteomyelitis in the posterior wall of the frontal sinus, as well as through the sphenoid and ethmoid sinuses. Intracranial extension of the infection by the venous route is common in paranasal sinus disease, especially in acute exacerbation of chronic inflammation.
After the injection of a contrast material, CT scans characteristically show the brain abscess as a hypodense center with a peripheral uniform enhancement ring. In the earlier cerebritis stages, CT scans show mild patchy enhancement with areas of low attenuation without enhancement. As the abscess forms, irregular rim of peripheral contrast enhancement is observed. After encapsulation, distinct enhancing rim with clear center is seen. Deep part of capsule is thinnest and towards cortex, it is thickest. In late capsule stage, cavity shrinks, capsule thickens, may become multiloculated and having ‘daughter’ abscesses.
On MRI, contrast enhancement with gadolinium helps differentiate the abscess, the enhancement ring, and the cerebral edema around the abscess. T1W images enhance the abscess capsule, and T2W images can demonstrate the edema zone around the abscess. Diffusion-weighted (magnetic resonance) imaging (DWI) can be used to differentiate between ring-enhancing lesions caused by brain abscess (hyperintense on DWI) from a malignant lesion (hypointense on DWI).
 
Differential Diagnosis
  • Resolving hematoma
  • Metastasis
  • Glioblastoma multiforme
  • Demyelination.
33
 
CASE-17
A 52-year-old female presenting with sudden onset headache followed by loss of consciousness.
zoom view
Figs 1.17A to D:
 
Findings
Plain CT axial image (A) of brain demonstrates hyperdense extraxial lesion with adjacent bony hyperostosis. MRI T1W (B), T2-FLAIR (C) showed heterogenous intensity mass extraaxial mass lesion with evidence of acute intratumoral and subarachnoid hemorrhage. Post-contrast T1W MR axial image (D) shows intense heterogeneous enhancement with dural tail.
 
Diagnosis
  • Meningioma with intratumoral/intracranial hemorrhage.34
 
Discussion
Incidence of a spontaneous intracranial hemorrhage in meningioma is rare (0.5–2.4%). Most common location is subarachnoid (54%) followed by subdural, intracerebral and intraventricular location.
Intraventricular, highly vascular and malignant histologic variants of meningiomas have increased propensity for hemorrhage.
Causes of hemorrhage include:
  • Rupture of abnormal vessels of the tumor
  • Direct vascular invasion by tumor cells
  • Stretching and rupture of subdural veins
  • Fragility of arterial and venous walls due to rapid tumor growth.
 
Differential Diagnosis
  • Gliosarcoma
  • Hemangiopericytoma.
35
 
CASE-18
A 5-year-old male child brought with case of two episodes of seizure like episode with loss of consciousness, generalized tonic clonic seizures.
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Figs 1.18A to G:
 
Findings
Magnetic resonance imaging brain T1W axial (A); axial T2W (B); axial T2 FLAIR (C) images demonstrate a supratentorial lobulated intraventricular (trigonal) mass lesion with adjacent vasogenic edema seen on right side which is hypointense on T1W and hyperintense on T2W with areas of cystic changes. Susceptibility weighted image (E) showed areas of dense calcification (confirmed on CT scanning; image not shown). Post-gadolinium T1W images (D and F) show enhancement of solid part of tumor. Hematoxylin and eosin36 stained high-field micrographic histopathology section (G) shows neoplastic cells having round to oval nuclei with granular chromatin and fibrillary cytoplasm with pseudorosette formation.
 
Diagnosis
  • Supratentorial ependymoma.
 
Discussion
  • Ependymomas are rare glial tumors derived from ependymal cells lining the ventricles of the brain, choroid plexus and the central canal of the spinal cord.
  • 80% of all tumors are located in infratentorial region. Supratentorial location is uncommon.
  • Peak incidences: fourth and fifth decades.
  • Incidence rate in first and second decades: 10 to 15%.
 
Imaging
Supratentorial ependymoma demonstrated heterogeneous signal intensity due to intratumoral hemorrhagic foci, calcification and necrosis. Tumor shows cystic changes resulting in T2W high signal intensity. On contrast administration tumor shows moderate to intense enhancement with ring-enhancement pattern.
The treatment of choice is total radical resection. Postoperative radiation therapy must be administered in every case of partially resected. The ‘prophylactic’ use of spinal irradiation is not necessary in supratentorial ependymomas of children and young adults.
 
Differential Diagnosis
  • Primitive neuroectodermal tumor
  • Astrocytoma (oligodendroglioma)
  • Supratentorial ependymoma
  • Pilocytic astrocytoma.37
 
CASE-19
A 55-year-old man presented with excruciating low backache.
zoom view
Figs 1.19A to I:
 
Findings
Magnetic resonance imaging sagittal T2W myelographic image (A), T2-TSE sagittal (B) and transverse (D to F) images of the lumbar spine show thickened, clumped cauda equine nerve roots, adhering to one another and to dural sac.
Non-enhanced T1W sagittal image (C) and fat-suppressed contrast-enhanced T1W sagittal (G) and transverse (H and J) images of the lumbar spine show heterogeneous enhancement of granulation tissue involving leptomeninges and encasing the cauda equine nerves.38
 
Diagnosis
  • Lumbar arachnoiditis.
 
Discussion
Arachnoiditis is a broad term denoting inflammation of the meninges and subarachnoid space one of the membranes that surround and protect the nerves of the central nervous system, including the brain and spinal cord.
Inflammation can sometimes lead to the formation of scar tissue and adhesions which can cause the spinal nerves to ‘stick’ together. This can be extremely painful especially if the last stage ‘Adhesive Arachnoiditis’ is diagnosed.
Infectious etiologies in arachnoiditis include bacterial, viral, fungal, and parasitic agents. Non-infectious inflammatory etiologies include surgery, intrathecal hemorrhage, and the administration of intrathecal agents, such as myelographic contrast media, anesthetics, and steroids.
 
Differential Diagnosis
  • Recurrent disc herniation
  • Disc fragments
  • Spinal canal stenosis
  • Spondylosis
  • Epidural fibrosis.