Info

The Migraine And Headache Program

Migraines Natural Treatments

Get Instant Access

Figure 25. Supratentorial astrocytoma. Heterogeneous, predominantly T2-hyperintense mass centered in the deep gray nuclei. Small areas of enhancement. (transaxial T1-WI with contrast, and T2-WI.

Figure 27. Large, left, hemispheric, irregular, heterogeneous, dense, enhancing PNET with cystic components and punctate calcifications. (CT, FLAIR, T1-WI with contrast)

■r /

V W

I

Figure 27. Large, left, hemispheric, irregular, heterogeneous, dense, enhancing PNET with cystic components and punctate calcifications. (CT, FLAIR, T1-WI with contrast)

Table 11. Sellar and suprasellar tumors

Tumor Type Location Imaging Appearance Other Features Figures

Table 11. Sellar and suprasellar tumors

Tumor Type Location Imaging Appearance Other Features Figures

Astrocytoma

Hypothalamus and/or optic chiasm

Lobulated hypodense solid mass |T1 and |T2 SI Variable enhancement If large, can be heterogeneous

Visual deficits and optic disc atrophy Endocrinopathy Associated with NF1

28

Craniopharyngioma

Along hypothalamic stalk between floor of third ventricle and pituitary gland Usually suprasellar; large tumors can extend beyond suprasellar area

Multicystic, suprasellar, enhancing mass with calcification Rarely intrasellar Variable T1 and |T2 SI

Headaches Visual deficits Endocrine dysfunction (e.g., diabetes insipidus, growth failure)

29, 30

Germinoma

Involve stalk and extend into hypothalamus

Well-defined, slightly heterogeneous mass Iso- or hyperdense JT1 and mixed T2 SI Enhancement

Diabetes insipidus is common

31

Granulomatous disease

(TB and sarcoid)

Hypothalamus and infundibulum

Enlarged infundibulum Enhancement

Hypothalamic-pituitary dysfunction

Hypothalamic hamartoma

Tuber cinereum of hypothalamus, between mammillary bodies

Well-defined oval mass

Isodense and isointense to gray matter

No enhancement

Precocious puberty Gelastic seizures Developmental delay

32

Î = increased; J = decreased; NF1 = neurofibromatosis type 1; SI = signal intensity

Î = increased; J = decreased; NF1 = neurofibromatosis type 1; SI = signal intensity

Tumor Type Location Imaging Appearance Other Features Figures

Langerhans cell histiocytosis

Hypothalamus, infundibulum and pituitary

Enlarged infundibulum Enhancement

Often indistinguishable from GCT, granulomatous process and lymphocytic hypophysitis

Hypothalamic-pituitary dysfunction

Lymphocytic hypophysitis

Anterior pituitary and hypothalamus

Enlarged hypothalamus and infundibulum Enhancement

Headache Visual deficit Hypothalamic-pituitary dysfunction

Pituitary adenoma

Pituitary gland (intrasellar) Large adenomas can extend into suprasellar compartment, and compress optic chiasm

Well-defined mass |T1 SI

Less enhancement than surrounding normal gland

Headaches Visual deficits Endocrine dysfunction (e.g., amenorrhea, Cushing's disease)

33

Rathke's cleft cyst

Pituitary gland (intrasellar)

Well-defined oval mass Variable T1 and T2 SI No enhancement

Headache Visual deficit Hypothalamic-pituitary dysfunction

34

Î = increased; J = decreased; GCT = germ-cell tumor; SI = signal intensity

Î = increased; J = decreased; GCT = germ-cell tumor; SI = signal intensity

Figure 28. Chiasmatic astrocytoma. Homogeneously enhancing suprasellar mass. The chiasm cannot be defined. (coronal T1-WI with contrast)

Figure 29. Craniopharyngioma. Lobu-lated hypodense suprasellar mass with peripheral calcifications. (transaxial CT)

Figure 31. Suprasellar germinoma with extension inferiorly along the pituitary stalk. (coronal T1-WI with contrast)
Figure 32. Hypothalamic hamartoma. Small nonenhancing nodule that is isointense to gray matter, and located in the hypothalamic region. (coronal T2-WI, sagittal T1-WI with contrast)
Pituitary Infundibulum

Figure 34. Rathke's cleft cyst. Well-defined oval focus of decreased enhancement in the midline upper pituitary gland, abutting the optic chiasm. (coronal T1-WI with contrast)

Table 12. Pineal region masses

Mass Location Imaging Appearance Other Features Figures

Table 12. Pineal region masses

Mass Location Imaging Appearance Other Features Figures

Germinoma

Pineal or suprasellar regions, and, rarely, deep gray nuclei Most common (>50%) pineal region tumor

See Table 11

Disseminate via CSF Pineal germinomas have

10:1 M:F ratio Can secrete placental alkaline phosphatase

35

Glioma

Quadrigeminal plate, or medial temporal or occipital lobes

Hypodense |T1 and |T2 SI Enhancement

Large parapineal gliomas can be difficult to distinguish from primary pineal tumors

Pineal cyst

Pineal gland

Well-defined homogeneous cyst

Isodense, T1 -isointense and fT2 SI relative to CSF

Peripheral rim of enhancement

Never causes hydrocephalus Uncommon in infants Non-neoplastic

36

Pineocytoma and pineoblastoma

Pineal parenchyma

Lobulated mass containing calcification

Enhancement

Hypodense

Isointense, or JT1 SI and isointense, or fT2 SI

Pineoblastomas are highly malignant, invasive and can spread via CSF

37

Teratoma

Pineal or suprasellar region, third ventricle, or midline posterior fossa

Heterogeneous mass with fat and calcification Heterogeneous T1 and T2 SI; SI due to fat Variable enhancement

Most are benign, but few can be highly malignant Male predominance

f = increased; J = decreased; CSF = cerebrospinal fluid; SI = signal intensity f = increased; J = decreased; CSF = cerebrospinal fluid; SI = signal intensity

Figure 35. Germinoma. Slightly heterogeneous, mildly enhancing T1-hypointense, T2-hyperintense mass in the pineal region. (transaxial T1-WI with contrast, and T2-WI)
Figure 36. Pineal cyst. Well-defined homogeneous (nonenhancing) T1-hypointense and T2-hyperintense cyst-like mass in the pineal region. (sagittal T1-WI, and transaxial T2-WI)

Figure 37. Pineo-blastoma causing noncommunicating hydrocephalus. (transaxial T1-WI, without and with contrast)

Figure 37. Pineo-blastoma causing noncommunicating hydrocephalus. (transaxial T1-WI, without and with contrast)

Table 13. Congenital brain malformations

Malformation

Clinical Features

Imaging Features

Other Associations

Figures

Agenesis of corpus callosum

Developmental delay Seizures

Chiari I (Inferior cerebellar tonsillar ectopia)

Chiari II

Headaches

Lower cranial-nerve palsies Swallowing difficulties Dysesthesias

Uniformly seen in association with myelomeningocele at birth Development delay Lower cranial nerve palsies leading to dysphagia or stridor

Absence of corpus callosum

Parallel configuration of lateral ventricles

Colpocephaly (enlarged atria and occipital horns of lateral ventricles) "High-riding" third ventricle Absence of cingulate sulcus Sagittal and coronal MR sequences helpful

Cerebellar tonsils > 5 mm below foramen magnum Small posterior fossa Hydrocephalus and syringohydromyelia may be present Consider CSF flow study

Small posterior fossa

Inferior cerebellar vermis displaced through the foramen magnum Hydrocephalus "Beaked" tectum Callosal hypogenesis Hypoplastic talx with gyri interdigitated across midline Cervicomedullary kink Large massa intermedia

Interhemispheric cyst 38

Chiari II

Dandy-Walker malformation Septo-optic dysplasia Neuronal migrational anomalies

Segmentation anomalies of 39

cervical spine Always evaluate for syringohydromyelia in spinal cord

Subependymal heterotopias 40

Aqueductal stenosis Hindbrain malformation associated with myelomeningocele

CSF = cerebrospinal fluid

Malformation

Clinical Features

Imaging Features

Other Associations

Figures

Dandy-Walker malformation

Gray matter heterotopias

Holoprosencephaly

Defined as a cystic malformation of the posterior fossa Macrocephaly Developmental delay Seizures Headaches

Seizures

Can be asymptomatic Can have additional mild motor and intellectual deficits

Varies with severity of malformation Dysmorphic facial features Midline facial clefts Hypotelorism Seizures

Developmental delay Hypothalamic-pituitary dysfunction

Large posterior fossa

High insertion of torcula

Vermian hypogenesis

Fourth ventricle communicates with large posterior fossa cyst Hydrocephalus

Nonenhancing nodules that are isointense to gray matter, and located along lateral ventricles or subcortical regions

Absent septum pellucidum Alobar type: severe Absent callosum, talx and interhemispheric fissure; monoventricle; fused thalami Semilobar type: intermediate Partially absent callosum, talx and interhemispheric fissure +/- thalamic fusion; monoventricle Lobar type: mild Near normal ventricles, talx, callosum and thalami

A spectrum of posterior fossa 41

anomalies that includes Dandy-Walker variant and mega cisterna magna Callosal hypogenesis Migrational anomaly

Callosal dysgenesis 42

Cerebellar malformations Gray matter in abnormal locations due to arrested radial neuronal migration

Trisomies 1 3 and 18 43

Failure of induction of the rostrobasal prosencephalon

Malformation

Clinical Features

Imaging Features

Other Associations

Figures

Lissencephaly ("Smooth brain") Abnormal neuronal migration

Polymicrogyria ("Too many small gyri")

Schizencephaly

Septo-optic dysplasia (de Morsier's Syndrome)

Seizures

Developmental delay

Seizures

Developmental delay

Seizures

Developmental delay Motor deficits

Variable

Hypoplasia of optic discs Hypothalamic-pituitary dysfunction

Lack of sulcation

Thickened cerebral cortex (pachygyria) Decreased white matter volume

Disruption of normal cortical organization Fine excessive irregularity of cortex, focal or diffuse

Occasional |T2 SI of underlying white matter Occasional calcification

Full thickness cleft, extending from pial surface to ventricle Cleft lined with gray matter

(and polymicrogyria) Involves one or both cerebral hemispheres Commonly in frontal or parietal lobes

Hypoplasia or absence of septum pellucidum Hypoplasia of optic nerves and chiasm

Congenital CMV infection 44

Callosal dysgenesis Congenital heart disease

Dense polymicrogyria can 45

mimic pachygyria Congenital CMV infection

Can be "open-lip" or "closed-lip," 46 depending on apposition of cleft's walls Distinguish from porencephaly, which is a cleft lined with gliotic white matter

Mild callosal dysgenesis Can be difficult to distinguish from lobar holoprosencephaly

Î = increased; CMV = cytomegalovirus t/i

Figure 38. Complete absence of the corpus callosum with abnormal parallel configuration of the lateral ventricles. (sagittal T1-WI)

Figure 39. Chiari I. Inferior herniation and "peg-like" configuration of the cerebellar tonsils. (sagittal T1-WI)

Figure 41. Dandy-Walker malformation. High insertion of the torcula with hypoplasia of the cerebellar vermis. (sagittal T1-WI)

Figure 40. Chiari II. Small posterior fossa with inferior herniation of the cerebellar tonsils, beaking of the tectum, towering of the vermis and hypoplasia of the falx. Small gray-matter heterotopias along the lateral margins of the ventricles. (sagittal T1-WI)

Figure 41. Dandy-Walker malformation. High insertion of the torcula with hypoplasia of the cerebellar vermis. (sagittal T1-WI)

Figure 43. Semilobar holoprosencephaly. Absent septum pellucidum separating the lateral ventricles. Dysgenesis of anterior corpus callosum. (sagittal and coronal T1-WI)

Figure 44. Lissencephaly. Diffuse lack of sulcation. Callosal agenesis. (transaxial T2-WI)

Figure 45. Polymicrogyria. Abnormal morphology of gyri in both frontal lobes. Excessive fine irregularity of cortex, consistent with dense polymicrogyria, mimicking pachygyria. (transaxial T2-WI)

Was this article helpful?

0 0
Naturally Cure Your Headaches

Naturally Cure Your Headaches

Are Headaches Taking Your Life Hostage and Preventing You From Living to Your Fullest Potential? Are you tired of being given the run around by doctors who tell you that your headaches or migraines are psychological or that they have no cause that can be treated? Are you sick of calling in sick because you woke up with a headache so bad that you can barely think or see straight?

Get My Free Ebook


Post a comment