Table 14 Continued

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Type

Features

Imaging Features

Figures

Neurofibromatosis type-2 (NF2)

Tuberous sclerosis complex (TSC; Bourneville^ disease)

Autosomal dominant Gene on chromosome 22 Bilateral vestibular schwannomas/

"acoustic neuromas" Few cafe au lait spots Cutaneous neurofibromas Cataracts Family history

Autosomal dominant Implicated genes on chromosomes 9 and 1 6 Classical triad: mental retardation, epilepsy, and adenoma sebaceum (angioti bromas, redd ish-brown nodular facial rash) Cutaneous lesions: truncal adenomata sebaceum, depigmented nevi ("ash-leaf spots" Retinal hamartomas Renal angiomyolipomas Cardiac rhabdomyomas Cystic lung disease (lymphangioleiomyomatosis)

BRAIN 51

Bilateral vestibular schwannomas (iso- or hypodense, isointense T1 and |T2 SI, enhance) Schwannomas of other cranial nerves

Multiple meningiomas (isodense, isointense T1 and T2 SI, enhance) SPINE

Multiple intra- or paraspinal schwanommas

Spinal cord ependymomas (JT1 and |T2 SI, enhance)

Meningiomas

Cord compression from tumors, +/- syringohydromyelia)

"Tubers" (cerebral hamartomas; hypo- or isodense, 52-54

T1 and T2 SI varies with age, "[calcification with age) Subependymal hamartomas (hyperdense nodules along ventricular surface, most commonly in region of caudate head; T1 and T2 SI varies with age, variable enhancement, "[calcification with age) Giant cell tumor (enlarging, enhancing subependymal nodule, most commonly at foramen of Monro; can cause hydrocephalus) White matter lesions (linear bands of |T2 SI) Retinal hamartomas (enhancing nodules, +/- calcification)

Î = increased; J = decreased; SI = signal intensity

Table 14. Continued

Type

Features

Imaging Features Figures

von Hippel-Lindau disease (retinocerebellar angiomatosis)

Autosomal dominant Gene on chromosome 3 Retinal angiomas CNS hemangioblastomas Renal cell carcinomas Pheochromocytomas Cysts of pancreas, liver, testes Family history

Hemangioblastomas (cerebellum > spinal cord » cerebrum; enhancing nodule with associated prominent flow voids and frequently nonenhancing cystic component) Syringohydromyelia due to spinal-cord hemangioblastomas

Sturge-Weber syndrome (encephalotrigeminal angiomatosis)

Most cases sporadic Congenital angiomatosis ot face, ocular choroids and leptomeninges Facial angioma or "port-wine stain" Seizures Hemiparesis

Glaucoma or buphthalmos Mental retardation

Gyral calcifications along affected cerebral hemisphere with underlying cortical atrophy (JT2 SI) Marked ipsilateral leptomeningeal and cortical enhancement Enlargement of ipsilateral choroid plexus, calvarium and sinuses

I = decreased; CNS = central nervous system; SI = signal intensity

Figure 47. NF1. Enhancing T1-hypointense mass along the optic chiasm. Enlargement of optic nerves. (sagittal T1-WI, without and with contrast)

Figure 49. NF1. Bilateral enhancing masses extending out through the lumbar neural foramina, consistent with neurofibromas. (transaxial T1-WI with contrast and fat saturation)

Figure 48. NF1. Areas of T2-hyper-in-tensity represent abnormal areas of my-elination. (coronal T2-WI)

Figure 48. NF1. Areas of T2-hyper-in-tensity represent abnormal areas of my-elination. (coronal T2-WI)

Figure 49. NF1. Bilateral enhancing masses extending out through the lumbar neural foramina, consistent with neurofibromas. (transaxial T1-WI with contrast and fat saturation)

Figure 50. NF1. Enhancing intradural and extramedullary nodules within the lumbar spinal canal, consistent with neurofibromas. (sagittal T1-WI with contrast and fat saturation)

Figure 51. NF2. Bilateral enhancing cerebellopontine angle masses extending into the internal auditory canals, consistent with bilateral vestibular schwannomas. (coronal T1-WI with contrast)

Figure 52. Tuberous sclerosis complex. Extensive calcifications. (transaxial CT)

Figure 54. Tuberous sclerosis with giant-cell tumor. Large enhancing intraventricular mass at the foramen of Monro, consistent with giant-cell tumor. (transaxial T1-WI with contrast)

Figure 53. Tuberous sclerosis complex. Multiple scattered T2-hyperintense foci, consistent with "tubers." (transaxial FLAIR)

Figure 54. Tuberous sclerosis with giant-cell tumor. Large enhancing intraventricular mass at the foramen of Monro, consistent with giant-cell tumor. (transaxial T1-WI with contrast)

Table 15. Intramedullary spinal masses

Mass Imaging Appearance Other Features Figures

Table 15. Intramedullary spinal masses

Mass Imaging Appearance Other Features Figures

Arteriovenous malformation

In acute presentation: hyperdense and T1-hyperintense parenchymal and/or subarachnoid hemorrhage Nidus present

Prominent flow voids within and around cord (dilated abnormal feeding arteries and draining veins) Aneurysms may be present

Two types:

Glomus: tight intramedullary nidus Complex/juvenile: enlarged vessels often occupy entire spinal canal

Demyelinating disease (e.g., ADEM, multiple sclerosis)

"Flame"-shaped JT1 and |T2 SI

Active lesion can enhance

Acute lesions can cause mild cord expansion

Lesions may not be contiguous

No syringohydromyelia

Consider obtaining MRI of brain to evaluate for additional demyelinating lesions

55

Syringomyelia

Severity ranges from dilation of the central canal to large eccentric fluid collection with internal incomplete septations I so intense to CSF on all sequences

Chiari II

Chiari I less common Hydrocephalus Spinal stenosis Tumors Tethered cord Prior cord injury

Traumatic spinal cord contusion

Acute contusions: JT1 and |T2 SI with cord expansion Hemorrhage may be present

Old injuries: volume loss with |T2 SI (myelomalacia) +/- syrinx

Other evidence of spinal trauma may be present: paraspinous soft tissue injury, fractures, loss of normal alignment

f = increased; J = decreased; ADEM = acute disseminated encephalomyelitis; CSF = cerebrospinal fluid; SI = signal intensity f = increased; J = decreased; ADEM = acute disseminated encephalomyelitis; CSF = cerebrospinal fluid; SI = signal intensity

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