Introduction To Neuroimaging

ARTICLE IN PRESS
REVIEW
Neurology Series, Editor, William J. Mullally, MD
Introduction to Neuroimaging
Elizabeth George, MD, Jeffrey P. Guenette, MD, Thomas C. Lee, MD
Department of Radiology, Brigham and Women’s Hospital, Boston, Mass.
ABSTRACT
Primary care physicians are often tasked with evaluating neurologic symptoms, and imaging plays a crit-
ical role in neurologic diagnoses. Neuroradiology routinely employs advanced imaging modalities, and hence,
determination of the appropriate imaging test and interpretation of findings in the clinical context can un-
derstandably be overwhelming. In this review article, we introduce resources that can guide physicians in
the selection of neuroimaging tests and summarize guidelines on contrast agent administration. Key con-
cepts on imaging techniques and terminology are reviewed, as is relevant for the primary care physician.
We then present an overview of the typical imaging manifestations of brain pathologies, including stroke,
traumatic injuries, infections, demyelinating and neurodegenerative processes, and neoplasms. Spine imaging
is often considered for the evaluation of degenerative, infectious, or neoplastic etiologies, and the typical
imaging findings in these scenarios are also summarized.
© 2017 Elsevier Inc. All rights reserved. • The American Journal of Medicine (2017) ■■, ■■–■■
KEYWORDS: Brain; CT; Head and neck; MRI; Neuroradiology; Spine
INTRODUCTION a test does not reflect high-value care, which included 3

Neurologic symptoms such as headache and low back pain neuroimaging scenarios, specifically, imaging for low back
are common reasons for patients to present to the primary pain, recurrent classic migraine, and simple syncope.4
care physician.1 Imaging plays a crucial role in the diagno- An understanding of imaging as it pertains to the diag-
sis of a wide range of neurologic disorders. However, there nosis and management of neurologic disorders will aid the
is often a lack of dedicated radiology training in medical school primary care physician in ordering the most appropriate ex-
and nonradiology residencies about the information provid- amination, interpreting the radiologists’ reports, determining
ed by different imaging modalities, determination of the the next steps in management, and making appropriate re-
appropriate imaging study, and interpretation of emergent ferrals to specialists. The purpose of this article is to review
findings.2 Moreover, neuroimaging routinely employs ad- the basic concepts of neuroimaging as is relevant to the primary
vanced modalities such as magnetic resonance imaging (MRI) care physician, specifically, the appropriateness of imaging
and is rapidly evolving in both technologic developments and tests, typical imaging techniques and terminologies, factors
the understanding of imaging manifestations of pathophysi- to consider prior to contrast agent administration, and the
ology. A large fraction of these advanced imaging studies are imaging findings of common pathologies.
requested by primary care physicians.3 Furthermore, over-
utilization of imaging resources has come under much scrutiny.
The American College of Physicians emphasizes appropri- APPROPRIATENESS OF IMAGING
ate use of diagnostic tests and identified 37 situations in which The American College of Radiology has established Appro-
priateness Criteria (https://acsearch.acr.org/list), which
summarize the literature on the role of imaging for a range
Funding: None. of neurologic manifestations and can serve as a guide for
Conflicts of Interest: The authors have no conflicts of interest. choosing the appropriate imaging test for specific clinical
Authorship: All authors had access to the data and a role in writing this presentations.5 In addition, there are diagnostic and manage-
manuscript. ment guidelines from organizations such as the American
Requests for reprints should be addressed to Elizabeth George, MD, De-
partment of Radiology, Brigham and Women’s Hospital, 75 Francis Street,
Neurologic Association and the American Heart Associa-
Boston, MA 02115. tion, which include recommendations on diagnostic and
E-mail address: egeorge6@partners.org interventional imaging studies.
0002-9343/$ - see front matter © 2017 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/j.amjmed.2017.11.014
Downloaded for Dept. Radiologi Kariadi (ksmradrsdk@gmail.com) at Dr Kariadi General Hospital Medical Center Department of Anaesthesiology from ClinicalKey.com by Elsevier
on March 15, 2018. For personal use only. No other uses without permission. Copyright ©2018. Elsevier Inc. All rights reserved.
ARTICLE IN PRESS
2 The American Journal of Medicine, Vol ■■, No ■■, ■■ 2017
IMAGING TECHNIQUES AND TERMINOLOGY independent risk factor for acute kidney injury.7 Patients with
Computed tomography (CT) scans of the head and spine are anuric end-stage renal disease on dialysis can safely receive
generally performed without contrast; administration of con- iodinated contrast media as there is no risk of further renal
trast can be considered if there is suspicion for intracranial damage. In patients with acute kidney injury, estimated glo-
metastases or spinal surgery complication, such as infec- merular filtration rate <30 mL/min/1.73 m2, or on dialysis,
tion, in patients who cannot undergo MRI. Spine CT certain classes of GBCA are contraindicated due to the risk
with intrathecal contrast (CT my- of nephrogenic systemic fibrosis.7
elography) is useful to assess the The effect of GBCA on a fetus is
CLINICAL SIGNIFICANCE unclear, and hence these should be
patency of the spinal canal and
neural foramen in patients with ra- • Evidence-based guidelines, such as the administered in pregnancy only
dicular symptoms when MRI is American College of Radiology Appro- when critical to the diagnosis, and
contraindicated or nondiagnostic. 6 requires informed consent.7 Re-
priateness Criteria, can guide physicians
On head CT, common causes of cently, gadolinium has been found
in choosing appropriate imaging tests.
hyperattenuation/hyperdensity to be deposited in the brain in pa-
(bright areas) are calcifications, • Study indication, renal function, preg- tients who have received multiple
hemorrhage, and iodinated con- nancy status, and prior allergies are doses of GBCA; clinical conse-
trast, while hypoattenuation/ factors to consider prior to administra- quences of this, if any, are
hypodensity (dark areas) is a tion of iodinated or gadolinium-based unknown.7
nonspecific finding that can be due contrast agents.
to infarct, mass, or edema. Brain
MRI typically includes diffusion- • Imaging is crucial to neurologic diag- IMAGING FINDINGS
weighted and susceptibility- noses, and typical imaging appearances
weighted imaging (SWI) or of common traumatic, infectious, in- Brain Pathologies
Gradient Recovery Echo (GRE) flammatory, vascular, and neoplastic Stroke. In patients with suspected
images in addition to the T1- and processes of the brain and spine are stroke, emergent CT of the head is
T2-weighted, T2-weighted fluid- summarized. performed prior to initiation of
suppressed (such as T2-fluid tissue plasminogen activator to
attenuation inversion recovery exclude intracranial hemorrhage.
[FLAIR]) sequences. Areas of high signal on diffusion- Hyperacute (<6 hours) infarcts are
weighted imaging with corresponding low signal on apparent not reliably detected on CT, although occasionally a “dense
diffusion coefficient maps are referred to as areas of low or vessel” sign is identified at the site of vascular occlusion. Emer-
restricted diffusivity and denote areas of infarct or high cel- gent noninvasive vascular imaging, such as CTA or MRA,
lularity. SWI/GRE images are particularly sensitive to is recommended prior to endovascular intervention to deter-
hemorrhage and calcifications. Spine MRI typically in- mine the site of occlusion. However, administration of tissue
volves T1- and T2-weighted images, and a fat-suppressed T2- plasminogen activator should not be delayed for vascular
weighted sequence such as STIR (short tau inversion recovery). imaging.8 MRI allows for both identification of hyperacute
Postcontrast images are acquired if there is concern for tumor infarcts as areas of restricted diffusivity and dating of in-
or infection. Regarding vascular imaging, CT angiography farcts based on the appearance on specific MRI sequences,
(CTA) has the advantage of superior spatial resolution, while such as high signal intensity on T2-FLAIR (typically >6 hours)
MR angiography (MRA) is often performed based on the phe- and contrast enhancement (typically >3 days).9,10
nomenon of flow-related enhancement (called “time-of- Embolic occlusive infarcts most commonly affect the
flight MRA”), without the need for contrast administration. middle cerebral artery distribution, whereas small lacunar in-
farcts are due to occlusion of deep perforating arteries and
have a predilection for the basal ganglia, pons, internal and
external capsule, and corona radiata (Figure 1). The pres-
CONTRAST CONSIDERATIONS ence of multiple infarcts in the anterior and posterior circulation
In patients with a known allergic reaction to iodinated CT of both hemispheres raises concern for a cardiac source of
contrast media, steroid premedication should be considered emboli (Figure 1). Systemic hypotension in the presence of
prior to administration.7 Allergic reactions to gadolinium- high-grade carotid stenosis/occlusion can result in “water-
based MRI contrast agents (GBCA) are very rare, but in shed” infarcts, which affect the border zones between the
patients with a known allergic reaction, it may be prudent to anterior and middle cerebral artery circulation in the frontal
premedicate with steroids and administer a different GBCA.7 lobes (Figure 1) or between the middle and posterior cere-
There is no cross-reactivity between GBCA and iodinated con- bral artery circulation in the posterior parietal lobes.11
trast media.7 CTA/MRA of the neck is often performed along with
In patients without acute kidney injury and with esti- vascular imaging of the brain to assess for atherosclerotic
mated glomerular filtration rate >30 mL/min/1.73 m2, there disease of the carotid vessels, quantified using the North
is little evidence that iodinated contrast media is an American Symptomatic Carotid Endarterectomy Trial or
ARTICLE IN PRESS
George et al Neuroimaging 3
Figure 1 Different distributions of infarct, all characterized by hyperintensity on diffusion-

weighted imaging. (A) Right middle cerebral artery territory infarct involving the basal ganglia
and right temporal lobe. (B) Lacunar infarct of the left corona radiata. (C) Watershed in-
farcts in the borderzone between the anterior cerebral artery and middle cerebral artery
circulation. (D) Infarcts in bilateral frontal lobes, suggesting cardioembolic phenomenon.
Asymptomatic Carotid Atherosclerosis Study criteria,10 and though previously associated with a high stroke risk of ~5%
for creating a roadmap of the cervical vessels for endovascular within 48 hours,14 aggressive management strategies have im-
intervention. Carotid stenosis can also be assessed using proved the prognosis.13
Doppler ultrasound based on peak systolic velocities.
Transient Ischemic Attack. Although classically, transient Trauma. Blunt or penetrating injury to the head can result
ischemic attack was defined based on the duration of symp- in hemorrhage in several compartments, such as subdural, epi-
toms (<24 hours), 30%-50% of these patients had evidence dural, subarachnoid, or parenchymal (Figure 2). Subdural
of infarction on imaging.12 Hence, the definition was updated hemorrhages are caused by tear of the bridging veins, while
to “a transient episode of neurological dysfunction caused by 90% of epidural hematomas are arterial from tear of the middle
focal brain, spinal cord, or retinal ischemia, without acute meningeal artery with associated skull fractures.15 The classic
infarction,”12 and brain imaging (preferably MRI) is recom- presentation of lucid interval followed by loss of conscious-
mended within 24 hours of symptom onset to exclude ness is seen in up to 20% of patients with epidural hematoma.16
infarction.12 Noninvasive imaging of the cervical and intra- Epidural hematomas warrant prompt recognition and close
cranial vessels (CTA, MRA, or carotid ultrasound/transcranial follow-up, as they can enlarge rapidly, requiring surgical
Doppler) is also routinely performed, demonstrating ≥50% evacuation;17 a classic exception being a small epidural he-
intra- or extracranial stenosis in ~23% patients.12,13 Al- matoma in the anterior aspect of the middle cranial fossa.
ARTICLE IN PRESS
Figure 2 Intracranial hemorrhage. Crescentic hyperdense appearance of a subdural hematoma (A) in contrast to
lenticular appearance of an epidural hematoma (B). (C) Hyperdense appearance of the basilar cisterns represent-
ing subarachnoid hemorrhage. (D) Right frontal parenchymal hemorrhage. (E) Susceptibility-weighted magnetic
resonance image demonstrates multiple foci of microhemorrhages (hypointense foci) at the gray-white junction,
corpus callosum, and right thalamus, consistent with diffuse axonal injury.
Diffuse axonal injury results from shear injury due to dif- intracranial aneurysms, with an estimated prevalence of 3%
ferential motion of the gray and white matter during (Figure 3).18 The American Heart Association recommends
acceleration or deceleration and typically results in loss of offering aneurysm screening with CTA or MRA for patients
consciousness at the time of impact. Initial head CT is often with polycystic kidney disease or ≥2 family members with
negative, and hence, diffuse axonal injury should be sus- intracranial aneurysm or subarachnoid hemorrhage.19 The de-
pected in a patient with discrepant clinical and imaging findings cision to intervene is based on the presentation, aneurysm size,
with a supporting mechanism of trauma. MRI SWI/GRE se- and patient risk scores.20 Patients who are medically managed
quence can usually identify diffuse axonal injury lesions in are typically followed with CTA or MRA within 6-12 months
the classic locations of gray-white junction, splenium and pos- of initial discovery and then yearly or every other year
terior body of corpus callosum, brain stem, basal ganglia, (Figure 3).19 Follow-up imaging is also indicated in pa-
internal capsule, and the superior cerebellar peduncle tients who have undergone surgical or endovascular repair,
(Figure 2). particularly those with high-risk features.19,20
Other Vascular. Nontraumatic parenchymal hemorrhage is Infection. Meningitis is diagnosed clinically based on ce-
often secondary to hypertension and classically involves the rebrospinal fluid analysis; imaging is generally not indicated
deep gray matter, brain stem, and cerebellum. The most and is often negative in early and successfully treated men-
common nontraumatic cause of subarachnoid hemorrhage is ingitis. Imaging may, however, be performed to rule out space-
a ruptured aneurysm. Widespread use of neuroimaging occupying intracranial lesions prior to a lumbar puncture, detect
has also resulted in increased detection of incidental source of infection such as sinusitis, or detect complica-
ARTICLE IN PRESS
Figure 3 Intracranial aneurysm. (A) Computed tomography angiography coronal maximum

intensity projection image demonstrates an aneurysm of the left internal carotid artery ter-
minus. (B) Magnetic resonance angiography demonstrates an aneurysm of the right middle
cerebral artery bifurcation.
tions such as abscess or hydrocephalus.10,21 Brain abscesses neoplasms classified based on histology and molecular
are often seen in patients with congenital heart disease, markers. This also includes a grading system, with Grades
intravenous drug use, or HIV/AIDS. These frequently occur 1 and 2 representing low-grade and Grades 3 and 4 repre-
at the gray-white junction and are characterized by rim- senting high-grade tumors.23 Intracranial tumors are broadly
enhancing lesions with surrounding vasogenic edema, central divided into extra-axial (outside the brain parenchyma) and
low diffusivity (Figure 4), and occasionally, a T2 hypointense intra-axial (within the brain parenchyma) lesions, with extra-
rim. These can rupture into the ventricle, causing ventricu- axial tumors accounting for a majority, the most common being
litis. Herpes simplex virus-1 is another common culprit of meningiomas. Meningiomas are dural-based masses that are
encephalitis, characterized by T2-FLAIR hyperintensity in- twice as common in women and are WHO Grade 1 in ~90%
volving the medial temporal lobe, insula, and cingulum, with of cases (Figure 5). A majority of the intra-axial neoplasms
possible associated gyriform low diffusivity, enhancement, are metastases, characterized as well-defined enhancing masses,
or hemorrhage.22 Empyema/abscess can also occur in the epi- typically at the gray-white junction.10 Glioblastoma, the most
dural or subdural spaces, identified by their central low common primary intra-axial neoplasm, is a WHO Grade 4
diffusivity, and are often secondary to sinusitis, otomastoiditis, tumor with poor median survival of 15 months. The typical
trauma, postsurgery, or untreated bacterial meningitis.10 appearance is of a heterogenous necrotic mass with periph-
eral enhancement and surrounding T2 hyperintensity, which
Neoplasm. The World Health Organization (WHO) 2016 clas- represents a combination of infiltrating nonenhancing tumor,
sification system has an exhaustive list of intracranial edema, and gliosis (Figure 5).24
Figure 4 Intracranial infection. Cerebral abscess (A-C) characterized by rim-enhancing mass (B) with central low
diffusivity (C) and surrounding vasogenic edema (A).
ARTICLE IN PRESS
Figure 5 Intracranial neoplasms. (A) Extra-axial dural-based mass consistent with a me-
ningioma. (B) Multiple enhancing foci, predominantly at gray-white junction, representing
metastases. (C, D). Peripherally enhancing centrally necrotic mass of the corpus callosum
with marked surrounding T2 hyperintesity representing glioblastoma.
Neurodegenerative Diseases. Along with clinical assess- Vascular or multi-infarct dementia is characterized by mul-
ment, structural imaging can play a role in diagnosing tiple areas of white matter infarcts and deep gray matter
various neurodegenerative causes of dementia and lacunar infarcts.10
excluding alternative etiologies such as hydrocephalus, in-
tracranial hemorrhage, or mass. Alzheimer’s disease, the Demyelinating Disorders. Multiple sclerosis is the most
most common cause of neurodegenerative dementia,25 is common demyelinating disorder in the United States and is
characterized by atrophy of the hippocampi and medial diagnosed based on the McDonald criteria. This criteria re-
temporal lobes. On 18F-fluorodeoxyglucose-positron emis- quires evidence of lesions disseminated in both time
sion tomography, the earliest abnormality is hypometabolism (appearance of a new lesion or simultaneous presence of both
in the posterior cingulate cortex with later involvement enhancing and nonenhancing lesions) and space (juxtacortical,
seen of the hippocampi, medial temporal lobes, precuneus, periventricular, infratentorial, or spinal cord lesions).27,28 These
and lateral temporoparietal lobes. The frontal lobes are lesions appear on MRI as flame-shaped areas of T2
involved in advanced Alzheimer’s disease (Figure 6).26 hyperintensity that enhance during active demyelination and
ARTICLE IN PRESS
Figure 6 Alzheimer’s disease. (A) Magnetic resonance imaging demonstrates bilateral temporal lobe atrophy. 18F-
fluorodeoxyglucose-positron emission tomography demonstrates marked hypometabolism of the temporal lobes (B)
and posterior cingulate cortex and precuneus (C).
often appear at the callososeptal interface (called “Dawson GBCA administration is generally reserved for concerns of
fingers”) (Figure 7).10 Acute disseminated encephalomyeli- malignancy or infection.
tis is an immune-mediated demyelinating process, commonly
affecting children, which can mimic the appearance of tumors. Infection. Discitis and vertebral osteomyelitis are second-
Monophasic acute disseminated encephalomyelitis lesions typ- ary to either hematogenous dissemination from a distant site
ically resolve by 3 months.10,29 or direct extension from recent spinal surgery. These pa-
tients typically present with back pain, fever, and elevated
Spine Pathologies inflammatory markers. On MRI, there is T1 hypointensity and
Degenerative disease. The majority of patients presenting T2/STIR hyperintensity involving the end plates, with later
with low back pain do not require imaging. Imaging should involvement of the discs and vertebral bodies.31 There is gen-
be considered if there is concern for cauda equina syn- erally associated enhancement of the bone marrow, discs,
drome, malignancy, fracture, or infection, or if there is little prevertebral and paraspinal soft tissues (Figure 9). MRI is
or no improvement after 6 weeks of physical therapy.6 MRI also crucial in detecting complications such as epidural or
is superior to CT in patients with persistent radiculopathy, paraspinal abscess or phlegmon, leptomeningeal involve-
who are candidates for intervention, or have prior history of ment, or displacement of the thecal sac. Contrast enhancement
surgery.6 CT is beneficial in the postoperative setting to assess is beneficial in differentiating diffusely enhancing phleg-
for hardware complications. For chronic neck pain, x-ray study mon from centrally nonenhancing abscess, which is crucial
of the cervical spine is the recommended initial diagnostic in determining medical vs surgical management.31 On follow-
examination, with MRI reserved for cases with neurologic up, MRI findings can lag behind clinical improvement.32
symptoms, persistent pain despite conservative manage-
ment, or concern for infection or malignancy. 30 MRI Trauma. Although CT is the preferred imaging modality in
demonstrates the extent of disc degeneration, facet arthropa- the setting of trauma,6,30 MRI can be complementary if there
thy, and spinal canal and neural foraminal stenosis (Figure 8). are neurologic deficits, concerns for ligamentous injury, or
Figure 7 Multiple sclerosis. Multiple flame-shaped areas of T2-fluid attenuation inversion recovery hyperintensity
in the periventricular white matter (A), callososeptal interface (B), “Dawson fingers”, and peripheral T2 hyperin-
tense lesion in the cervical spinal cord (C).
ARTICLE IN PRESS
Figure 8 Lumbar disc degenerative disease. Lumbar spine magnetic resonance imaging shows extruded disc frag-
ment (A, B) causing severe spinal canal stenosis. (C) Normal appearance of the spinal canal at an adjacent level
for comparison.
to assess for bone marrow edema to differentiate acute from Extramedullary intradural lesions include meningiomas and
chronic compression fractures.6 The evaluation of stability of nerve sheath tumors such as neurofibroma or schwannoma.
spinal fractures includes a combination of clinical and ra- Metastatic disease can also infiltrate the arachnoid and pia
diologic assessment. The spinal column is divided into anterior, mater (leptomeninges) focally or diffusely (Figure 10). The
middle, and posterior columns, and involvement of more than most common extradural/epidural neoplastic lesion is me-
one column is generally considered an unstable injury.10 The tastasis, often extending into the anterior epidural space from
thoracolumbar injury classification and severity score guides vertebral body metastases (Figure 10) and can cause nar-
treatment decisions and is based on the morphology of frac- rowing of the thecal sac. The associated vertebral body
ture, neurologic involvement, and involvement of the posterior metastases are characterized by T1 hypointensity, T2/STIR
ligamentous complex.33 hyperintensity, and heterogenous enhancement.
Neoplasm. Tumors of the spinal canal are generally classi- Inflammatory lesions. Guillain-Barré syndrome is an
fied based on their location into intramedullary (within immune-mediated polyneuropathy, often preceded by an in-
the spinal cord), extramedullary intradural, and extradural fection. MRI can support this diagnosis by demonstrating
lesions. The most common intramedullary spinal tumors are enlarged, enhancing nerve roots, usually at the cauda equina,
astrocytoma, ependymoma, and hemangioblastoma. 10 and exclude alternative etiologies such as myelopathy, or
Figure 9 Discitis/osteomyelitis. Magnetic resonance imaging study of the lumbar spine fat-suppressed T2 se-
quence (A) demonstrates hyperintensity of the disc and the adjacent vertebral bodies (arrows) with epidural soft
tissue (arrowhead), which demonstrates peripheral enhancement consistent with abscess (B, C, arrowhead). Note
paraspinal soft tissue enhancement (C, asterisk).
ARTICLE IN PRESS
Figure 10 Spinal metastases. (A) T2 hyperintensity of multiple thoracic vertebral bodies

representing vertebral metastases with epidural extension (arrow) causing spinal canal ste-
nosis and deformation of the cord (B). (C) Diffuse leptomeningeal enhancement (arrowhead)
in this patient represents leptomeningeal carcinomatosis.
infiltrative or compressive radiculopathy.34 Transverse my- Image-Guided Intervention

elitis manifests as rapidly progressive neurologic dysfunction There are many image-guided spine interventions per-
with edematous expansion of the cord and possible patchy formed for pain control, including facet injections, nerve
enhancement, typically extending over multiple vertebral body root blocks, and epidural steroid injections.37 Vertebral
levels and often involving the entire cross-section of the cord.35 augmentation procedures are often performed for osteopo-
Multiple sclerosis lesions commonly affect the cervical spinal rotic vertebral compression fractures, although there are
cord. These also demonstrate T2/STIR hyperintensity, but are mixed data on its benefit.38,39 Newer applications include
typically located peripherally (Figure 7), are <2 vertebral body CT- and MRI-guided ablation of head and neck and spine
segments in length, and rarely cause cord enlargement or tumors.40
enhancement.10
Head and Neck Pathologies CONCLUSION

Head and neck imaging is within the realm of neuroradiology Imaging is crucial to the diagnosis of many neurologic pa-
and includes CT and MRI with contrast, often performed for thologies encountered by the primary care physician. The key
evaluation of neck masses. The most common cause of neck concepts regarding radiologic techniques, terminology, and
mass in adults is lymphadenopathy, either inflammatory or common imaging manifestations as summarized in this article
metastatic.36 Other less frequent etiologies for neck masses will aid the primary care physician in identifying the appro-
include congenital, neoplastic, traumatic, and infectious/ priate imaging test, interpreting the study report, and
inflammatory (Figure 11). determining the next steps in patient management.
ARTICLE IN PRESS
Figure 11 Neck mass. (A, B) A 15-year-old girl presented with a painful neck mass. Com-
puted tomography scan of the neck with contrast demonstrates an abscess (arrow) in a right
cervical lymph node, corresponding to the neck swelling. (C, D) Sixty-seven-year-old man
with sudden-onset left neck swelling and pain, found to have asymmetric enlargement of
the left submandibular gland (dashed arrow) with surrounding fat stranding, representing
sialadenitis. Normal submandibular gland on the right (arrowhead).
References media/ACR/Files/Clinical-Resources/Contrast_Media.pdf. Accessed

1. Frese T, Druckrey H, Sandholzer H. Headache in general practice: fre- December 13, 2017.
quency, management, and results of encounter. Int Scholar Res Notices. 8. Powers WJ, Derdeyn CP, Biller J, et al. 2015 American Heart Association/
2014;2014:169428. American Stroke Association Focused Update of the 2013 Guidelines
2. Saha A, Roland RA, Hartman MS, Daffner RH. Radiology medical for the Early Management of Patients with Acute Ischemic Stroke Re-
student education: an outcome-based survey of PGY-1 residents. Acad garding Endovascular Treatment: a guideline for healthcare professionals
Radiol. 2013;20:284-289. from the American Heart Association/American Stroke Association.
3. Weilburg JB, Sistrom CL, Rosenthal DI, et al. Utilization Manage- Stroke. 2015;46:3020-3035.
ment of High-Cost Imaging in an Outpatient Setting in a Large Stable 9. Allen LM, Hasso AN, Handwerker J, Farid H. Sequence-specific MR
Patient and Provider Cohort over 7 Years. Radiology. 2017;284:766- imaging findings that are useful in dating ischemic stroke. Radiographics.
776. 2012;32:1285-1297, discussion 1297-1298.
4. Qaseem A, Alguire P, Dallas P, et al. Appropriate use of screening and 10. Nadgir R, Yousem D. Neuroradiology: The Requisites. 4th ed. Phila-
diagnostic tests to foster high-value, cost-conscious care. Ann Intern Med. delphia, PA: Elsevier, Inc.; 2017.
2012;156:147-149. 11. Mangla R, Kolar B, Almast J, Ekholm SE. Border zone infarcts: patho-
5. Appropriateness Criteria List. Vol 2017; 2017. Available at: https:// physiologic and imaging characteristics. Radiographics. 2011;31:1201-
acsearch.acr.org/list. Accessed December 7, 2017. 1214.
6. Patel ND, Broderick DF, Burns J, et al. ACR appropriateness criteria 12. Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of tran-
low back pain. J Am Coll Radiol. 2016;13:1069-1078. sient ischemic attack: a scientific statement for healthcare professionals
7. ACR Committee on Drugs and Contrast Media. ACR Manual on Con- from the American Heart Association/American Stroke Association Stroke
trast Media, Version 10.3. 2017. Available at: https://www.acr.org/-/ Council; Council on Cardiovascular Surgery and Anesthesia; Council
ARTICLE IN PRESS
on Cardiovascular Radiology and Intervention; Council on Cardiovas- 27. Igra MS, Paling D, Wattjes MP, Connolly DJA, Hoggard N. Multiple
cular Nursing; and the Interdisciplinary Council on Peripheral Vascular sclerosis update: use of MRI for early diagnosis, disease monitoring and
Disease. The American Academy of Neurology affirms the value of this assessment of treatment related complications. Br J Radiol.
statement as an educational tool for neurologists. Stroke. 2009;40:2276- 2017;90:20160721.
2293. 28. Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for mul-
13. Amarenco P, Lavallee PC, Labreuche J, et al. One-year risk of stroke tiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol.
after transient ischemic attack or minor stroke. N Engl J Med. 2011;69:292-302.
2016;374:1533-1542. 29. Pohl D, Alper G, Van Haren K, et al. Acute disseminated encephalo-
14. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke myelitis: updates on an inflammatory CNS syndrome. Neurology.
statistics—2015 update: a report from the American Heart Associa- 2016;87:S38-S45.
tion. Circulation. 2015;131:e29-e322. 30. Newman JS, Weissman BN, Angevine PD, et al. ACR Appropriate-
15. Rincon S, Gupta R, Ptak T. Imaging of head trauma. Handb Clin Neurol. ness Criteria Chronic Neck Pain. Vol 2017; 2013. Available at: https://
2016;135:447-477. acsearch.acr.org/docs/69426/Narrative/. Accessed December 13, 2017.
16. Winn RH. Youmans and Winn Neurological Surgery. Philadelphia, PA: 31. Kumar Y, Gupta N, Chhabra A, Fukuda T, Soni N, Hayashi D. Mag-
Elsevier, Inc.; 2017. netic resonance imaging of bacterial and tuberculous spondylodiscitis
17. Zangbar B, Serack B, Rhee P, et al. Outcomes in trauma patients with with associated complications and non-infectious spinal pathology mim-
isolated epidural hemorrhage: a single-institution retrospective cohort icking infections: a pictorial review. BMC Musculoskelet Disord.
study. Am Surg. 2016;82:1209-1214. 2017;18:244.
18. Vlak MH, Algra A, Brandenburg R, Rinkel GJ. Prevalence of unruptured 32. Gillams AR, Chaddha B, Carter AP. MR appearances of the temporal
intracranial aneurysms, with emphasis on sex, age, comorbidity, country, evolution and resolution of infectious spondylitis. AJR Am J Roentgenol.
and time period: a systematic review and meta-analysis. Lancet Neurol. 1996;166:903-907.
2011;10:626-636. 33. Lee JY, Vaccaro AR, Lim MR, et al. Thoracolumbar injury classifica-
19. Thompson BG, Brown RD Jr, Amin-Hanjani S, et al. Guidelines for tion and severity score: a new paradigm for the treatment of thoracolumbar
the Management of Patients With Unruptured Intracranial Aneurysms: spine trauma. J Orthop Sci. 2005;10:671-675.
a guideline for healthcare professionals from the American Heart 34. Burns TM. Guillain-Barre syndrome. Semin Neurol. 2008;28:152-
Association/American Stroke Association. Stroke. 2015;46:2368- 167.
2400. 35. Weidauer S, Wagner M, Nichtweiss M. Magnetic resonance imaging and
20. Burkhardt JK, Benet A, Lawton MT. Management of small incidental clinical features in acute and subacute myelopathies [e-pub ahead of print].
intracranial aneurysms. Neurosurg Clin N Am. 2017;28:389- Clin Neuroradiol. 2017 Jun 30. doi:10.1007/s00062-017-0604-x.
396. 36. Pynnonen MA, Gillespie MB, Roman B, et al. Clinical practice guide-
21. Brouwer MC, van de Beek D. Management of bacterial central nervous line: evaluation of the neck mass in adults. Otolaryngol Head Neck Surg.
system infections. Handb Clin Neurol. 2017;140:349-364. 2017;157:S1-S30.
22. Bulakbasi N, Kocaoglu M. Central nervous system infections of her- 37. Palmer WE. Spinal injections for pain management. Radiology.
pesvirus family. Neuroimaging Clin N Am. 2008;18:53-84, viii. 2016;281:669-688.
23. Louis DN, Perry A, Reifenberger G, et al. The 2016 World Health Or- 38. Buchbinder R, Osborne RH, Ebeling PR, et al. A randomized trial of
ganization Classification of Tumors of the Central Nervous System: a vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med.
summary. Acta Neuropathol. 2016;131:803-820. 2009;361:557-568.
24. Alexander BM, Cloughesy TF. Adult glioblastoma. J Clin Oncol. 39. Li L, Ren J, Liu J, et al. Results of vertebral augmentation treatment
2017;35:2402-2409. for patients of painful osteoporotic vertebral compression fractures: a
25. Alzheimer’s Association. 2013 Alzheimer’s disease facts and figures. meta-analysis of eight Randomized Controlled Trials. PLoS One.
Alzheimers Dement. 2013;9:208-245. 2015;10:e0138126.
26. Nasrallah IM, Wolk DA. Multimodality imaging of Alzheimer disease 40. Guenette JP, Tuncali K, Himes N, Tatli S, Lee TC. Spine cryoablation:
and other neurodegenerative dementias. J Nucl Med. 2014;55:2003- a multimodality image-guided approach for tumors adjacent to major
2011. neural elements. AJNR Am J Neuroradiol. 2016;37:2396-2399.

Introduction To Neuroimaging

Încărcat de

Informații document

Titlu original

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

Introduction To Neuroimaging

Încărcat de

Drepturi de autor:

Formate disponibile

ARTICLE IN PRESS

KEYWORDS: Brain; CT; Head and neck; MRI; Neuroradiology; Spine

INTRODUCTION a test does not reflect high-value care, which included 3

Figure 1 Different distributions of infarct, all characterized by hyperintensity on diffusion-

Figure 3 Intracranial aneurysm. (A) Computed tomography angiography coronal maximum

Figure 10 Spinal metastases. (A) T2 hyperintensity of multiple thoracic vertebral bodies

infiltrative or compressive radiculopathy.34 Transverse my- Image-Guided Intervention

Head and Neck Pathologies CONCLUSION

References media/ACR/Files/Clinical-Resources/Contrast_Media.pdf. Accessed

S-ar putea să vă placă și