Chapter A16: Atlas of Neuroimaging

Limbic encephalitis (Chap. 90). Coronal (A, B), axial fluid-attenuated inversion recovery (FLAIR) (C, D), and axial T2-weighted (E) MR images demonstrate abnormal high signal involving the bilateral mesial temporal lobes (arrowheads) including the hippocampi (left greater than right) without significant mass effect (arrows). There was no enhancement on postgadolinium images (not shown).

Hashimoto’s encephalopathy (Chap. 132). Axial FLAIR (A) demonstrates focal area of abnormal high signal involving the gray and white matter in the left frontal lobe (arrows). There is also a small area of abnormal high signal in the precentral gyrus. Axial T1-weighted images (B, C) pre- and postgadolinium demonstrate cortical/pial enhancement in the region of high signal on FLAIR.

Glioblastoma multiforme (Chap. 86). Axial nonenhanced CT (A) shows an ill-defined lesion in the right cerebral hemisphere (arrows). Internal hyperdensities represent hemorrhagic foci (arrowheads). Axial T2 (B) and postcontrast T1 (C) weighted MRI demonstrate a peripherally enhancing right parietal lesion (arrows), with necrosis (*).

Pilocytic astrocytoma (Chap. 86). Axial T2-weighted and T1-weighted postgadolinium images (A, B) show a cystic lesion with peripheral enhancement and an enhancing solid component located in the posterior fossa (arrows). These findings are suggestive of a pilocytic astrocytoma. Note that the lesion exerts mass effect on the fourth ventricle, which is compressed (curved arrows).

Brainstem glioma (Chap. 86). Axial T2 FLAIR MRI (A) demonstrates increased T2 signal and marked enlargement of the pons (large arrows), which engulfs the basilar artery (small arrow). These findings are characteristic of brainstem glioma. At the time of diagnosis, these lesions are typically low grade without abnormal enhancement, as shown by axial postcontrast T1-weighted image (B).

Fourth ventricle ependymoma causing hydrocephalus (Chap. 86). Unenhanced axial CT images (A, B) demonstrate an expansile mass lesion, isodense with brain parenchyma, filling the fourth ventricle (arrows) and causing obstruction of cerebrospinal fluid flow, dilation of the lateral ventricles, and hydrocephalus (curved arrows). The hypoattenuation within periventricular white matter bilaterally represents transependymal flow (arrowheads). C. Axial T1-weighted postgadolinium MRI confirms the presence of a heterogeneously enhancing mass filling the fourth ventricle (arrows), which is suggestive of ependymoma.

Midline teratoma (Chap. 86). Sagittal T1-weighted (A) and axial T2-weighted (B) MRI demonstrate a large midline suprasellar cystic mass, with fluid (*) and fat and hair follicles (arrowheads). Nonenhanced CT axial (C) image shows cystic change (*) and fatty attenuation (arrowhead).

Colloid cyst of the third ventricle (Chap. 86). Sagittal T2-weighted MRI (A) demonstrates a cystic lesion in the region of the Foramina of Monro with low signal related to mucinous content (arrow). Axial T1-weighted postgadolinium MR image (B) demonstrates no internal enhancement or mural nodules (arrow).

Tuber cinereum hamartoma (Chaps. 86 and 374). Sagittal T1-weighted (A), axial T2-weighted (B), and sagittal T1-weighted postgadolinium (C) MRI demonstrate a well-circumscribed hypothalamic mass (arrowheads) with signal intensity similar to gray matter and no postcontrast enhancement.

Pituitary microadenoma (Chap. 373). Sagittal (A) and coronal (B) postcontrast T1-weighted MRIs demonstrate a small circumscribed nodule in the left pituitary gland (arrows).

Neurofibromatosis type 1 (Chap. 86). Axial T2 FLAIR MRI (A, B) demonstrates multiple hyperintense lesions involving the brainstem and basal ganglia (arrows) as well as deep cerebellar hemispheres (arrowheads). Sagittal and corona T1-weighted postcontrast MRI (C, D) shows enlargement of the optic chiasm with an area of enhancement on the left, representing an optic pathway glioma (arrows). Coronal STIR MRI (E) shows thoracolumbar scoliosis and a large paravertebral plexiform neurofibroma (arrows).

Neurofibromatosis type 2 (Chap. 86). Axial T1-weighted postcontrast MRI (A, B) shows enhancing expansible lesions in the bilateral cerebellopontine cisterns extending in the internal auditory canals, consistent with vestibular schwannomas (arrows), as well as in the bilateral prepontine cistern, consistent with trigeminal schwannomas (arrowheads). Coronal axial T1-weighted image postgadolinium (C) demonstrates an intensely enhancing dural-based lesion typical for a small meningioma (arrow). Sagittal (D, E) T1-weighted images postgadolinium show intradural, extramedullary lesions, suggestive of multiple spinal schwannomas (small arrows). The flat dural-based lesion may represent a spinal meningioma (arrowhead). Axial T1-weighted image postgadolinium (F) shows an enhancing intramedullary lesion, most consistent with an ependymoma (curved arrow).

Tuberous sclerosis (Chap. 86). Coronal T2-weighted MRI (A) shows multiple T2 hyperintense lesions in a cortical and subcortical distribution (arrows). Coronal and axial postcontrast T1-weighted image (B, C) demonstrates an expanding nodule with intense enhancement in the proximity of the right foramen of Monro, consistent with a subependymal giant-cell astrocytoma (SEGA) (arrowheads). Surveillance T1-weighted image (D) and postcontrast T1-weighted image with fat saturation (E) show multiple bilateral renal lesions with signal intensity of fat, consistent with angiomyolipomas (small arrows).

Neurocutaneous melanosis (Chap. 72). Coronal T1-weighted MRI (A–D) shows multiple lesions with intrinsic increased T1 signal in the bilateral amygdalae, right superior temporal gyrus, right cerebellar hemisphere, and right medial occipital cortex (arrows). Sagittal and axial T1-weighted images of the spine (E, F) show intradural, extramedullary lesions, also with intrinsic increased T1 signal, due to malignant melanoma (arrows).

Vertebral metastasis (Chap. 86). Sagittal T2-weighted (A), T1-weighted (B), and post-contrast T1-weighted with fat saturation (C) demonstrate a well-circumscribed bone lesion with increased T2 signal, low T1 signal, and intense enhancement (arrow). The central areas of hypoenhancement represent necrosis (*).

Retropharyngeal soft tissue mass (Chaps. 14 and 86). Sagittal T1-weighted MRI demonstrates a hyperflexion fracture with retropulsion of the posterior wall in the canal at C5 and C6 (arrow). There is also a large retropharyngeal hematoma (^*). The distance from the posterior wall of the airway to the anterior wall of the vertebral body should not measure >6 mm at C2 or >20 mm at C6 (mnemonic “6 at 2 and 20 at 6”).

Multiple myeloma (Chaps. 14 and 72). Axial noncontrast CT image (A) demonstrates multiple lytic lesions (*) involving the sacrum and iliac bones bilaterally and marked osteoporosis evidenced by a coarse trabecular pattern (arrow). Sagittal reformatted CT image (B) demonstrates a large lytic lesion replacing the posterior elements of the upper thoracic spine (*) and multilevel compression fractures in the thoracic and lumbar spine (arrows).

Brain abscesses (Chap. 135). Axial T2 FLAIR (A), T2-weighted (B), susceptibility-weighted imaging (C), diffusion-weighted imaging (D), ADC map (E), and postcontrast T1-weighted (F) MRI demonstrate bilateral brain abscesses, with well-defined contrast enhancing capsules (arrowheads), susceptibility effect from iron-rich inflammatory cells (short arrows), internal restricted diffusion (*) reflecting pus, and peripheral vasogenic edema (arrows).

Central nervous system tuberculosis (Chap. 173). Axial T2-weighted MRI (A) demonstrates multiple lesions (arrows) with peripheral high signal and central low signal, located predominantly in the cortex and subcortical white matter, as well as in the basal ganglia. Axial T1-weighted MR images postgadolinium (B, C) demonstrate ring enhancement of the lesions (arrows) and additional lesions in the subarachnoid space (arrowheads). Sagittal T2-weighted MR image of the cervical spine (D) demonstrates a hypointense lesion in the subarachnoid space at the level of T5 (arrow). Sagittal T1-weighted postgadolinium MRI of the cervical spine (E) demonstrates enhancement of the lesion in the subarachnoid space at the level of T5 (arrow).

Neurosyphilis (Chaps. 133, 134, and 177): Case I. Axial T2-weighted MRIs (A, B) demonstrate well-defined areas of abnormal high signal in the basal ganglia bilaterally and in a wedge-shaped distribution in the right parietal lobe (arrows). Axial (C, D) T1-weighted images postgadolinium. Coronal (E, F) T1-weighted images postgadolinium demonstrate irregular ring enhancement of the lesions (arrows).

Neurosyphilis (Chaps. 133, 134, and 177): Case II. Axial T2-weighted MRI (A) demonstrates a dural-based, peripherally hyperintense and centrally hypointense lesion located lateral to the left frontal lobe (arrow). Axial (B) and coronal (C) T1-weighted MRIs postgadolinium demonstrate peripheral enhancement of the lesion (arrows).

Histoplasmosis of the pons (Chap. 207). Axial FLAIR (A) and T2-weighted (B) MRIs demonstrate a low signal mass in the right pons (arrows) with surrounding vasogenic edema. Axial T1-weighted MRI postgadolinium (C) demonstrates ring enhancement of the lesion in the right pons (arrow). Of note, there was no evidence of restricted diffusion (not shown).

Coccidiomycosis meningitis (Chap. 208). Axial postcontrast CT (A) and axial (B) and coronal (C) T1-weighted MRIs postgadolinium demonstrate enhancement of the perimesencephalic cisterns (arrows), as well as the sylvian and interhemispheric fissures.

Candidiasis in a newborn (Chap. 211). Axial T2-weighted MRI (A) demonstrates multiple punctate foci of low signal diffusely distributed in the brain parenchyma (arrowhead). Axial T1-weighted MRIs postgadolinium (B, C) demonstrate marked enhancement of the lesions (arrowheads). Apparent diffusion coefficient (ADC) map (D, E) demonstrates restricted diffusion of water molecules in the lesions (arrowheads).

Central nervous system (CNS) aspergillosis (Chap. 212). Axial FLAIR MRIs (A, B) demonstrate multiple areas of abnormal high signal in the basal ganglia as well as cortex and subcortical white matter (arrows). There is also abnormal high signal in the subarachnoid space adjacent to the lesions (arrowheads) that can correspond to blood or high protein content. Axial T2-weighted MRIs (C, D) demonstrate intrinsic low signal in the lesions (arrows), suggesting the presence of blood products. Some of the lesions also show vasogenic edema. Coronal (E) and axial (F) T1-weighted MRIs postgadolinium demonstrate peripheral enhancement of the lesions (arrows).

Invasive sinonasal aspergillosis (Chap. 212). Axial T2-weighted MRI (A) demonstrates an irregularly shaped low signal lesion involving the left orbital apex (arrow). B. T1-weighted image pregadolinium demonstrates low signal in left anterior clinoid process (arrow). C. T1-weighted image postgadolinium demonstrates enhancement of lesion (arrow).

Behçet’s disease (Chap. 357). Axial FLAIR MRI demonstrates abnormal high signal involving the anterior pons (arrow); following gadolinium administration, the lesion was nonenhancing (not shown). Brainstem lesions are typical of Behçet’s disease, caused primarily by vasculitis and in some cases demyelinating lesions.

Neurosarcoid (Chap. 360): Case I. Coronal (A) and axial (B) T1-weighted images postgadolinium with fat suppression demonstrate a homogeneously enhancing well-circumscribed mass centered in the left Meckel’s cave (arrows).

Neurosarcoid (Chap. 360): Case II. Axial (A, B) and sagittal (C) T1-weighted images postgadolinium with fat suppression demonstrate a homogeneously enhancing mass involving the hypothalamus and the pituitary stalk (arrows).

Neurosarcoid (Chap. 360): Case III. Axial FLAIR images (A–E) demonstrate abnormal high signal and slight expansion in the midbrain, dorsal pons, and pineal region (arrows) without significant mass effect. Sagittal T1-weighted images postgadolinium (F) with fat suppression demonstrate abnormal enhancement in the midbrain, dorsal pons, and pineal region (arrows).

Neurosarcoid (Chap. 360): Case IV. Axial T2-weighted images (A–D) demonstrate numerous areas of abnormal hyperintensity involving the corpus callosum, left internal capsule and globus pallidus, bilateral cerebral peduncles, bilateral gyrus rectus, right frontal lobe periventricular white matter, and patchy areas in bilateral temporal lobes. T1-weighted images postgadolinium (E–H) demonstrate abnormal enhancement of those areas with high T2 signal.

Histiocytosis (Chap. 374). Sagittal T1-weighted image (A) demonstrates enlargement of the pituitary stalk (arrow) and absence of the posterior pituitary intrinsic T1 hyperintensity (arrowhead). Sagittal and coronal T1-weighted images postgadolinium (B, C) demonstrate enhancement of the pituitary stalk and infundibulum (arrows).

Bilateral gray-matter heterotopia (Chap. 418). Coronal (A) and axial (B) T1-weighted MRI demonstrates an abnormal thin layer of heterotopic gray matter in the posterior white matter bilaterally (arrowheads).

Middle cerebral artery stenosis (Chaps. 419 and 420). Time-of-flight (TOF) MR angiography (MRA) (A, B) reveals narrowing within the left M1 segment that is likely secondary to atherosclerosis (arrows).

Lacunar infarction (Chaps. 419 and 420). MRI demonstrates a focus of increased signal on T2 FLAIR weighted image (A), increased signal on diffusion-weighted image (B), and low ADC values (C) in the left thalamus (arrows).

Acute pontine infarct (Chaps. 419 and 420). Axial unenhanced CT (A) does not depict any abnormality. Axial T2 FLAIR weighted MRI (B) demonstrates a focal area of mild hyperintensity in the left pons (arrowhead) and axial diffusion-weighted MRI (C) and ADC map (D) demonstrate restricted diffusion representing cytotoxic edema (arrowheads).

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) (Chap. 420). Axial T2-weighted MRIs (A, B) demonstrate multiple patchy areas of abnormal high signal in the periventricular white matter (arrows). Coronal FLAIR MRI (C, D) demonstrates multiple patchy areas of abnormal high signal in the periventricular white matter bilaterally, including the temporal lobes (arrows). In some of these areas, there are small areas of tissue loss (encephalomalacia) (arrowheads).

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) (Chaps. 420 and 441). Axial T2 FLAIR MRI (A, B) shows areas of increased T2 signal involving the cortex and subcortical white matter in the posterior right frontal lobe and anterior left temporal lobe, consistent with edema (arrows). Axial diffusion-weighted images (C, D) show reduced diffusion from cytotoxic edema, consistent with infarcts (arrows). MR spectroscopy of the right frontal lesion (E) demonstrates markedly increased lactate (arrow), an expected finding in infarction regardless of etiology. However, MR spectroscopy of the normal-appearing contralateral brain parenchyma (F) shows mildly elevated lactate (arrow), which is suggestive of a mitochondrial disorder.

CNS vasculitis (Chap. 420). Axial noncontrast CT (A) demonstrates a large hyperdense intraparenchymal hematoma surrounded by hypodense vasogenic edema in the right parietal lobe (arrow). Axial T2-weighted MRI (B) demonstrates a large hypointense intraparenchymal hematoma surrounded by hyperintense vasogenic edema in the right parietal lobe (arrow). Conventional angiography (C) demonstrates multiple segments of intracranial arterial narrowing (arrows), some of which have associated adjacent areas of focal arterial dilatation. These abnormalities are suggestive of vasculitis.

Cerebral arteriopathy due to ACTA2 mutation (Chaps. 419 and 420). 3D Time-of-flight (3D-TOF) MR angiography (A) reveals narrowing of the intracranial arteries (arrowheads) and fusiform dilatation of the distal internal carotid arteries (arrows). Axial FLAIR weighted MRI (B) demonstrates multiple areas of gliosis and encephalomalacia (arrowheads) predominantly in the watershed zones bilaterally.

Superior sagittal sinus thrombosis (Chaps. 420 and 421). Noncontrast CT of the head (A) demonstrates increased density in the superior sagittal sinus, suggestive of thrombosis (arrow), and small linear hyperdensities in some temporal lobe sulci, suggestive of subarachnoid hemorrhage (arrowheads). Axial T1-weighted MRI (B) demonstrates absence of flow void in the superior sagittal sinus, suggestive of thrombosis. Coronal FLAIR images (C, D) demonstrate areas of abnormal high signal involving the gray and the subcortical white matter of the right frontal and left parietal lobes, as well as the adjacent sulci. These findings are suggestive of vasogenic edema with subarachnoid hemorrhage (arrowheads). Diffusion-weighted images (E, F) and ADC maps (G, H) demonstrate restricted diffusion of the abnormal areas on FLAIR, suggestive of infarct. Phase-contrast venography of the brain (I) demonstrates absence of signal in the superior sagittal sinus down to the torcular herophili, and left transverse sinus and jugular vein. Axial (J) and coronal (K) T1-weighted images postgadolinium demonstrate a filling defect in the superior sagittal sinus, suggestive of thrombosis.

Arteriovenous malformation (Chap. 421). Axial (A) and coronal (B) postcontrast T1MRI demonstrate a large AVM involving the right cerebral hemisphere. There are multiple tortuous vessels (arrowheads) and large abnormal draining veins (arrows). Right cerebral hemisphere atrophy is evident. Sagittal digital subtraction angiography (C) demonstrates the nidus (arrowheads) and early filling draining veins (arrows), skipping the capillary system.

Multiple cavernomas (Chap. 421). Axial susceptibility-weighted images (A–D) show multiple foci of susceptibility involving the bilateral cerebral hemispheres, pons, and left cerebellum, which in a young patient most likely represents multiple cavernomas (arrows). These lesions have variable signal intensity on T2-weighted (E) and T1-weighted MRI (F), related to the different stages of hemoglobin degradation (arrows). Cavernomas are not seen on the time-of-flight MR angiography (G); thus these are designated as angiographically occult vascular malformations. Of note, in elderly patients, amyloid angiopathy may have a similar appearance.

Sturge-Weber syndrome (Chap. 421). Coronal T1-weighted MRI (A) shows enlargement of the sulci in the left parietal lobe, consistent with brain parenchymal volume loss (arrows). Axial susceptibility-weighted imaging shows susceptibility effect in this region, consistent with calcifications (arrows). Coronal and axial T1-weighted images postgadolinium (C, D) show increased leptomeningeal enhancement (arrows) and enlargement of the left choroid plexus (curved arrow).

Von Hippel–Lindau (VHL) (Chap. 309). Axial postcontrast T1-weighted images (A–C) demonstrate multiple enhancing nodules in the posterior fossa (arrows). Sagittal postcontrast T1-weighted image (D) shows vascular flow voids within the enhancing nodule in the region of the foramen of Magendie (arrow), indicating increased vascularity. Surveillance axial T2-weighted MRI of the abdomen (E) shows multiple small pancreatic cysts (arrowheads). This patient did not have an endolymphatic sac tumor, renal cell carcinoma, neuroendocrine pancreatic tumor, or pheochromocytoma, all of which may also occur in von Hippel–Lindau disease.

Sickle cell disease and moyamoya disease (Chaps. 420 and 421). Axial T2-weighted MRI (A, B) shows multiple small areas of encephalomalacia from prior infarcts in the watershed zones between the anterior and middle cerebral artery territories (small arrows). There is also an area of edema involving the left basal ganglia from an evolving subacute infarct (arrow). An axial diffusion-weighted image (C) with corresponding ADC map (D) shows an area of restricted diffusion in the right frontoparietal region, consistent with an acute infarct (arrows). Time-of-flight MR angiography (E) shows absence of flow in the distal internal carotid arteries and proximal middle cerebral arteries (arrows) due to moyamoya disease. Also note that this patient is status post–bilateral encephalo-duro-arterio-synangiosis (EDAS) (arrowheads), a surgical procedure to create indirect anastomosis between branches of the external carotid artery with distal branches of the middle cerebral artery.

Hemiplegic migraine (Chap. 422). Axial noncontrast perfusion MRI using an arterial spin labeling technique (A) demonstrates decreased cerebral blood flow to the left hemisphere (arrows) in a patient with right hemiparesis associated with migraine symptoms. No abnormality was seen on T2-weighted images, diffusion-weighted images, or time-of-flight MR angiography (B–D) to suggest stroke.

Multiple system atrophy (Chap. 428). Axial T2-weighted MRI (A) reveals symmetric poorly circumscribed abnormal high signal in the middle cerebellar peduncles bilaterally (arrowheads). Sagittal T1-weighted MRI (B) demonstrates pontine atrophy and enlarged cerebellar fissures as a result of cerebellar atrophy (arrows).

Huntington’s disease (Chap. 428). Axial noncontrast CT (A) demonstrates symmetric bilateral severe atrophy involving the caudate nuclei, putamen, and globus pallidi bilaterally with consequent enlargement of the frontal horns of the lateral ventricles (arrows). There is also diffuse prominence of the sulci indicating generalized cortical atrophy. Axial (B) and coronal (C) FLAIR images demonstrate bilateral symmetric abnormal high signal in the caudate and putamen. Coronal T1-weighted image (D) demonstrates enlarged frontal horns with abnormal configuration. Also note diffusely decreased bone marrow signal, which could represent anemia or myeloproliferative disease.

Nonketotic hyperglycemic hemichorea (Chap. 428). Axial nonenhanced CT (A, B) demonstrate hyperdensity of the left basal ganglia (arrowheads). Findings tend to be contralateral to the body side affected by hemiballistic, hemichoreic movements. This finding should not be confused with hemorrhage.

Bell’s palsy (Chap. 433). Axial T1-weighted images postgadolinium with fat suppression (A–C) demonstrate diffuse smooth linear enhancement along the left facial nerve, involving the second and third segments (genu, tympanic, and mastoid) within the temporal bone (arrows). Note that there is no evidence of a mass lesion. A potential pitfall for facial nerve enhancement in the stylomastoid foramen is the enhancement of the stylomastoid artery that enters the foramen and supplies the tympanic cavity, the tympanic antrum, mastoid cells, and the semicircular canals. Coronal T1-weighted images postgadolinium with fat suppression (D, E) demonstrate the course of the enhancing facial nerve (arrows). Although these findings are highly suggestive of Bell’s palsy, the diagnosis is established on clinical grounds.

Lyme disease (Chaps. 181 and 433). Axial T1-weighted postgadolinium MRI (A, B) demonstrate contrast enhancement of the bilateral trigeminal (CN V) (arrowheads) and oculomotor nerves (CN III) (short arrows).

Spinal cord infarction (Chap. 434). Sagittal T2-weighted MRI of the lumbar spine (A) demonstrates poorly defined areas of abnormal high signal in the conus medullaris and mild cord expansion (arrow). T1-weighted MRI of the lumbar spine postgadolinium (B) demonstrates mild enhancement (arrow). Sagittal diffusion-weighted MRI of the lumbar spine (C) demonstrates restricted diffusion (arrow) in the areas of abnormal high signal on the T2-weighted image (A).

Acute transverse myelitis (Chap. 434). Sagittal T2-weighted MRI (A) demonstrates abnormal high signal in the cervical cord extending from C1 to T1 with associated cord expansion (arrows). Sagittal T1-weighted MRI postgadolinium (B) demonstrates abnormal enhancement in the posterior half of the cord from C2 to T1 (arrows).

B₁₂ deficiency myelopathy (Chap. 434). Sagittal T2-weighted (A) and axial T2-weigthed (B) MRI demonstrate high signal involving the posterior columns of the cervical spine (arrows).

Epidural hematoma (Chap. 435). Axial noncontrast CT (A) demonstrates a high-density epidural collection in the cervical spine (^*), which is consistent with acute hemorrhage. Also noted is mass effect on the spinal cord (arrowheads). Sagittal reformatted CT image (B) demonstrates the extension of the acute epidural hematoma (^*) and a disk bulge (arrowhead), which further contributes to spinal canal narrowing. CT is the imaging procedure of choice to detect acute hematoma.

Subdural hematoma (Chap. 435). Sagittal T2-weighted MRI (A) and axial noncontrast T1-weighted MRI (B) demonstrate subdural collection in the lumbosacral region (^**). Note that the epidural fat is compressed but not involved (arrow).

Chronic and acute subdural hematomas with midline shift (Chaps. 300 and 435). Chronic subdural hematoma with rebleeding. Axial noncontrast CT (A, B) demonstrates a right subdural collection (*) with chronic hypodense component (white*) and acute hyperdense component (black*). Also note significant mass effect on the right lateral ventricle and a right-to-left midline shift (arrows).

Multiple sclerosis (Chap. 436). Axial T2-weighted MRI (A, D) and axial T2 FLAIR MRI (B, E) demonstrate multiple hyperintense lesions involving the periventricular and subcortical white matter (arrows). Although not always present, the appearance of a “lesion within a lesion” (arrowheads) is typical of demyelinating disease. Axial T1-weighted postcontrast MRI (C, F) shows partial enhancement of the lesion (arrows), which is often peripheral, incomplete, and “C-shaped” (curved arrow).

Multiple sclerosis of the spinal cord (Chap. 436). Sagittal T2-weighted MR demonstrates multiple areas of increased signal within the spinal cord (arrows), consistent with demyelinating lesions.

Acute disseminated encephalomyelitis (ADEM) (Chap. 436). Axial T2-weighted (A) and coronal FLAIR (B) images demonstrate abnormal areas of high signal involving predominantly the subcortical white matter of the frontal lobe bilaterally and left caudate head (arrows). Following administration of gadolinium, corresponding axial (C) and coronal (D) T1-weighted images demonstrate irregular enhancement consistent with blood-brain barrier breakdown and inflammation; some lesions show incomplete rim enhancement, typical for demyelination (arrows).

Baló’s concentric sclerosis (a variant of multiple sclerosis) (Chap. 436). Coronal FLAIR MRI (A) demonstrates multiple areas of abnormal high signal in the supratentorial white matter bilaterally. The lesions are ovoid in shape, perpendicular to the orientation of the lateral ventricles, and with little mass effect. Axial (B) and sagittal (C–E) T2-weighted MRIs demonstrate multiple areas of abnormal high signal in the supratentorial white matter bilaterally, as well as the involvement of the body and splenium of the corpus callosum and the callosal-septal interface (arrowhead). Some of the lesions reveal concentric layers, typical of Baló’s concentric sclerosis (arrows). Sagittal (F) and axial (G, H) T1-weighted MRIs postgadolinium demonstrate abnormal enhancement of all lesions with some of the lesions demonstrating concentric ring enhancement (arrows).

Bilateral optic neuritis (neuromyelitis optica) (Chap. 437). Coronal STIR weighted MRI (A) demonstrates high signal and thickening of both optic nerves (arrowheads). Coronal (B) and axial (C) T1-weighted postgadolinium MRI demonstrates bilateral optic nerve enhancement (arrowheads).

Myelitis (neuromyelitis optica) (Chap. 437). Sagittal T2-weighted MRI demonstrates a large lesion with increased signal and cord swelling from edema extending from C4-C5 to T3-T4 (*).

Brachial plexopathy (Chap. 438). Axial (A), sagittal (B), and coronal (C, D) short tau inversion recovery (STIR). MRIs demonstrate abnormal enlargement and abnormal high signal involving the right C6, C7, and C8 nerve roots, and the trunks and divisions that originate from these roots (arrows). Diffusion-weighted MRI (E) demonstrates abnormal reduced diffusion within the right C6, C7, and C8 nerve roots and their corresponding trunks and divisions (arrow). These findings are compatible with radiation-induced brachial plexopathy.

Metachromatic leukodystrophy (Chap. 438). Axial T2WI (A) MRI demonstrates bilateral symmetrical confluent areas of periventricular white matter signal changes with a “tigroid pattern” (*), sparing the subcortical U fibers (arrows). Axial diffusion (B) and ADC maps (C) demonstrate restricted diffusion of water (arrows) reflecting cytotoxic edema.

Leigh’s disease (subacute necrotizing encephalomyelopathy) (Chap. 441). Axial T2-weighted MRI (A, B) demonstrates increased T2 signal involving the substantia nigra (white arrows) and dorsal midbrain (black arrows), as well as the putamen bilaterally (curved arrows). This is a common pattern for the mitochondrial disorder Leigh’s disease secondary to cytochrome oxidase (CO IV) deficiency.

Krabbe’s disease (Chap. 411). Axial and coronal T2-weighted MRIs (A, B) show increased T2 signal involving predominantly the posterior white matter bilaterally (arrows) with sparing of the subcortical U-fibers (arrowheads). MR spectroscopy of the left parietal white matter (C) shows markedly decreased N-acetylaspartate (large arrow) and increased lactate/lipids (small arrow), consistent with severe neuronal injury.

X-linked adrenoleukodystrophy (Chap. 411). Axial unenhanced CT (A) demonstrates areas of attenuation involving the posterior white matter bilaterally (arrows). Axial T2 FLAIR MRI (B) displays increased T2 signal consistent with edema (arrows). Axial T1-weighted image postgadolinium (C) shows peripheral enhancement of the parietal lesions bilaterally (arrows). These findings are typical of adrenoleukodystrophy.

Hepatic encephalopathy (Chap. 301). Axial T1-weighted MRI (A, B) shows increased intrinsic T1 signal involving the basal ganglia bilaterally, particularly the globus pallidus (arrows).

Guillain-Barré syndrome (Chap. 439). Axial precontrast T1-weighted MRI (A) and axial and sagittal T1-weighted postgadolinium (B, C) images show thickening and increased enhancement of the anterior roots of the cauda equina (arrows).

Anterior dens dislocation (Chap. 14). Sagittal CT demonstrates the tip of the dens below the anterior arch of C2 (arrow), indicating anterior dislocation.

C2 facet fracture (Chap. 14). Axial CT demonstrates fracture line along the C2 facet (arrow).

Compression fracture (Chap. 14). Sagittal T2-weighted MRI demonstrates compression fracture of C7 (^*) and high signal within the spinous processes of C6-C7 (arrows) and to lesser degree C5-C6. This is suggestive of interspinous ligament injury. Note the pad under the patient’s neck to maintain neck alignment during the scanning time.

Jefferson fracture (Chap. 14). Axial CT demonstrates four fracture lines (arrows) separating C1 in four parts. Jefferson fracture is usually caused by axial impact to the head such as diving in shallow water.

Ligament injury after trauma (Chap. 14). Coronal CT reconstruction demonstrates abnormal asymmetry between the dens and the lateral masses of C1 indicating transverse ligament rupture.

Odontoid fracture (Chap. 14). Sagittal CT demonstrates disruption of the main reference cervical lines. (1): Anterior vertebral body line; (2): posterior vertebral body line; (3): spinolaminar line.

Pathologic fracture (Chap. 14). Sagittal T1-weighted MRI (A) demonstrates wedge-shaped T6 vertebral body (arrow). Sagittal postcontrast T1-weighted MRI (B) depicts tumor extension into the epidural space and the involvement of the posterior arch (^*), which are highly suggestive of metastatic or primary bone tumor.

Sacral insufficiency fracture (Chap. 14). Axial T2-weighted MRI (A) and T1-weighted MRI (B) demonstrate symmetric high T2 and low T1 signal involving the sacral alae longitudinally (arrows).

Teardrop fracture (Chap. 14). Sagittal CT (A) demonstrates fracture line separating the anteroinferior corner of C6 (arrow). Sagittal T2-weighted MRI (B) displays cord injury (arrow).