CONTENTS OF THIS CHAPTER

• Introduction
• Radiologic anatomy
  • Cisterns
  • CT anatomy overview
  • Vascular distributions
• CT radiology
  • CT basics
  • Approach to reading a CT scan
• MRI
  • Understanding the sequences
    • T1
    • T1 with contrast
    • T2 & FLAIR
    • DWI & ADC
    • T2* (GRE & SWI)
  • Hematoma evolution on MRI
  • Approach to reading an MRI
• Selected neuroimaging differentials
  • Leptomeningeal enhancement
  • Dural enhancement
  • Gyral enhancement
  • Periventricular enhancement & ventriculitis
  • Solitary enhancing mass
  • Ring enhancing lesion(s)
  • U-fibers
• Podcast
• Questions & discussion
• Pitfalls

TOPICS IN NEURORADIOLOGY

• Anatomic problems:
  • Hydrocephalus
• Infection:
  • Brain abscess
  • Meningitis
  • Ventriculitis
• Inflammatory:
  • Tumefactive multiple sclerosis
• Myelopathy
  • MOG-antibody related diseases
  • Neuromyelitis optica spectrum disorders
• Oncologic
  • PCNSL (primary CNS lymphoma)
• Toxic/metabolic injuries:
  • Anoxic brain injury
  • Carbon monoxide
  • Hepatic encephalopathy
  • Hyperammonemic encephalopathy
  • Hypoglycemia
  • Methanol
  • Uremic encephalopathy
  • Wernicke encephalopathy
• Trauma:
  • Diffuse axonal injury
  • Epidural hematoma
  • Subdural hematoma
• Vascular:
  • Occlusion:
    • AIS (acute ischemic stroke)
    • CVT (cerebral venous thrombosis)
  • Hemorrhage:
    • ICH (intracerebral hemorrhage)
    • SAH (subarachnoid hemorrhage)
  • Vascular tone dysregulation:
    • PRES (posterior reversible encephalopathy syndrome)
    • RCVS (reversible cerebral vasoconstriction syndrome)

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introduction

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Most of the information about neuroradiology is integrated within individual chapters on various different conditions.  So this chapter is a repository of various, sundry remaining bits of information.  Prepare to be underwhelmed.

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cisterns

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cisterns 

• A  Cistern of the laminae terminalis.
• B  Chiasmatic cistern (aka suprasellar cistern).
• C  Interpeduncular cistern.
• D  Ambient cistern.
• E  Quadrigeminal cistern (aka superior cistern).
• F  Cerebellopontine cistern.
• G  Prepontine cistern (aka pontine cistern).
• H  Lateral cerebellomedullary cistern.
• I  Cisterna magna (aka cerebellomedullary cistern).  (Image courtesy of Dr. Coenraad Hattingh, Radiopaedia).

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CT anatomy overview

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vascular distributions

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CT basics

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HU (Hounsfield units)(31485116)

• Air:  -1000
• Fat:  -50 to -100
• Water:  zero
• White matter:  ~30
• Grey matter:  ~40
• Acute hemorrhage:  ~50-70
• Soft calcification:  60-80
• Dense calcification:  200-400
• Bone:  700-3,000
• Metal:  4000

selected windows

• Stroke windows to accentuate the grey/white differentiation:
  • Grey/white differentiation may be more easily identified with narrow windowing of the CT scan, to accentuate differences between grey and white matter (e.g., a CT window width of 8 and a window level of 32 HU).(31589578)  Other authors recommend a width 80 HU, level of 40 HU. (Wijdicks, 2019)  Some imaging programs have a stroke window setting built into the software.  
  • Stroke windows may also help clarify whether there is loss of grey/white differentiation following anoxic brain injury.
• Subdural window for extra-axial bleeding:
  • Width of 200 HU, level of 50 HU. (Wijdicks, 2019)

appearance of hematoma on CT scan

• (1) Acute blood is hyperdense (in the absence of anemia).
• (2) As blood clots, it becomes even more hyperdense (within hours of hemorrhage, lasting for several days).
• (3) Over the ensuing month, the density decreases.
  • First blood becomes isodense, then it ultimately becomes hypodense.
  • Reduction in density begins at the edges of the hemorrhage.

contrasted CT

• Entities which can be detected via a contrast-enhanced CT scan:
  • Focal lesions (e.g. tumors, abscess).
  • Vascular malformation (e.g., arteriovenous malformations).
• However, MRI is generally superior for these entities.

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approach to reading a CT scan

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things to look for when surveying the head CT scan in an ICU patient:  

blood

• Acute blood accumulations will be bright on CT scan.

cisterns

• Effacement or asymmetry may reveal mass effect, herniation, or hydrocephalus.
• Some key cisterns:
  • Quadrigeminal cistern:  behind the top of the midbrain.
  • Ambient cistern (aka circummesencephalic cistern):  surrounding the midbrain.
  • Suprasellar cistern:  superior to the pituitary fossa.

ventricles

• Evaluate lateral ventricles, third and fourth ventricles, look for:
• (1) Dilation may be evidence of hydrocephalus.
• (2) Effacement may reveal mass effect of surrounding brain tissue.
• (3) Intraventricular hemorrhage.

brain

• Look for asymmetry.
• Look for blurring of the grey/white border (evidence of global anoxia, or focal infarction).
• Focal hypodensity may reflect edema.

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T1

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features of T1

• Basic properties:
  • Fat & myelin are bright (White matter is white; grey matter is grey).
  • Water is dark.
• Pathological brightness:
  • Paramagnetic substances:
    • Subacute hematoma.
    • Copper, calcium, iron, melanin (e.g., metastatic melanoma).
  • Fat (including myelin).
  • Some proteinaceous material.
• Pathological darkness:
  • Chronic, fluid-filled lesions (similar to CT scan).
  • Edema, demyelination.
  • Chronic hematoma.

utility of T1

• T1 provides the greatest level of fine anatomic detail.
• Useful for obtaining further definition of abnormalities detected using other sequences.
• Rarely, may highlight specific pathologies (e.g., copper deposition in Wilson's disease).
• Useful as a background to determine whether a lesion enhances with gadolinium.  If there is a bright signal on the T1 with contrast, this reflects contrast enhancement only if the signal is absent in the plain T1 images.

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T1 with contrast

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• Contrast enhancement reflects active disruption of the blood-brain barrier.
• Causes of contrast enhancement include:
  • Tumors.
  • Wernicke encephalopathy.
  • Infection (e.g., meningitis).
  • Demyelination (e.g., multiple sclerosis, acute demyelinating encephalomyelitis).
• Various patterns of contrast enhancement are discussed further below:
  • Leptomeningeal enhancement
  • Dural enhancement
  • Gyral enhancement
  • Periventricular enhancement & ventriculitis
  • Solitary enhancing mass
  • Ring-enhancing lesion(s)

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T2 & FLAIR

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T2

• Basic features:
  • Fat is dark
  • Water is bright
  • Flow in vessels is dark
• Pathological brightness:
  • Any type of edema:
    • Cytotoxic edema of ischemic stroke.
    • Vasogenic edema (metastases, abscess, inflammation).
    • Interstitial edema due to hydrocephalus.
  • Demyelination, axonal loss.(Albin 2022)
  • Hyperacute hematoma, or late subacute hematoma.
  • Subacute to chronic infarcts.(Albin 2022)
• Pathological darkness
  • Fat; protein-rich masses.
  • Paramagnetic substances (iron, copper, melanin, calcium).
  • Acute hematoma or early-subacute hematoma.
  • Air.
•  Utility:
  • Good for detection of most lesions (but not terrific at finding lesions abutting the ventricles).
  • Useful for evaluating vasculature.
  • May provide high anatomic detail for abnormalities of the CSF spaces.

FLAIR (fluid attenuation inversion recovery)

• FLAIR is fundamentally extremely similar to T2, but with the CSF within the ventricles appearing black.
• Utility is generally similar to T2, with the following differences:
  • (1) Lesions abutting the ventricles or cortex are easier to see.
  • (2) FLAIR may improve grey/white differentiation.
  • (3) FLAIR is more sensitive for early detection of ischemic changes.(31485117)
  • (4) FLAIR is able to detect subarachnoid blood.
• FLAIR is often the single best sequence to survey for brain pathology.

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DWI & ADC

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DWI (diffusion-weighted imaging)

• Notable causes of bright signal on DWI: (Albin 2022)
  • Acute ischemic stroke (the ischemic core of the stroke is bright on DWI 📖).
  • Thick purulent material (within an abscess or subdural empyema).  This helps differentiate abscesses from necrotic tumors (which do not show diffusion restriction).(31485117)
  • Hematoma that is either hyperacute or late-subacute (similar to the appearance of hematoma on T2 sequences).(11754324) 
  • Seizure-related cortical restriction.
  • Hypoxic-ischemic injury.
  • Tumefactive necrosis.
  • Lymphoma, or high-grade glioma.
  • Creutzfeldt-Jakob disease.
  • Epidermal cysts.
• DWI represents T2 with superimposed bright signals that indicate restricted diffusion – which is often an indicator of cytotoxic edema (e.g., ischemia).  The most notable use of DWI is for the diagnosis of acute ischemic stroke.
• DWI images must always be compared to the T2 and ADC images.
  • If the bright signal is similar in DWI and T2 sequences, then this doesn't necessarily represent cytotoxic edema (but instead it could reflect vasogenic edema present on the T2 image, aka “T2 shine-through”).
  • If a bright signal is present on DWI that isn't as prominent on T2, then this indicates cytotoxic edema (true diffusion restriction).
  • ADC is even better at verifying the presence of cytotoxic edema (see below).

ADC (apparent diffusion coefficient)

• ADC is another way to help sort out true diffusion restriction (i.e., true cytotoxic edema – typically reflective of a stroke) from background vasogenic edema present on the T2 images.
  • True cytotoxic edema will have dark (low) ADC values.
  • Vasogenic edema will have high (bright) ADC values.

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GRE and SWI

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general features

• MRI sequences used to detect paramagnetic substances (blood, calcium, metals), which appear black.
• These sequences are largely used to look for hemorrhage.  All stages of hemorrhage appear dark (unlike T1 and T2 sequences, where the appearance of blood varies over time).
• There may be susceptibility blooming artefact, wherein signals are larger than the actual structure being imaged.  This can be useful to highlight small areas of hemorrhage or calcification.
• SWI is a more modern version of GRE, with greater sensitivity.

clinical utility

• Detection of hemorrhage, including small hemorrhages (e.g., microbleeds in the context of diffuse axonal injury from traumatic brain injury, or amyloid angiopathy).
• Detection of thrombus within the context of CVT (cerebral vein thrombosis).

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hematoma evolution on MRI

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Metabolism of hemoglobin leads to characteristic changes in hematoma appearance over time:

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approach to reading an MRI

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The best approach may be to synchronize 4-6 sequences and examine them together.  The sequences obtained will vary somewhat, depending on local practice patterns and how the study was protocoled (e.g., a STAT stroke-protocol MRI might focus on FLAIR, DWI, and ADC).

general approach:

1. FLAIR images are often a good place to start.  Vasogenic edema is bright on FLAIR, so this will highlight many common pathologies.
2. DWI images may be evaluated next.  DWI highlights cytotoxic edema, so pathology which is considerably brighter on DWI than on FLAIR suggests cytotoxic edema (e.g., ischemic stroke).  A dark signal on the ADC can be used to confirm the presence of cytotoxic edema.
3. T1 can be used to examine the fine anatomic detail of any lesions identified.
4. T1 with contrast can evaluate whether any lesions have caused disruption in the blood-brain barrier (revealed in the form of contrast enhancement, when compared to the T1 images).
5. SWI or GRE images are highly sensitive for blood.  This may be useful to identify blood within lesions seen on other sequences, or to find microhemorrhages which are too subtle to see on the other sequences.

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leptomeningeal enhancement

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The leptomeninges refers to the combination of the pia mater and arachnoid which are immediately adjacent to the brain.  Radiologically, enhancement appears to fill the sulci and cisterns:  

causes of diffuse leptomeningeal enhancement

• Meningitis or meningoencephalitis (bacterial, viral, tuberculous, fungal, chemical).(28466277)
• Leptomeningeal carcinomatosis.
• Subarachnoid hemorrhage.(28466277)
• Post-operative or post-traumatic (delayed finding).
• 💡 Leptomeningeal enhancement following lumbar puncture is rare.(23122257)  Enhancement due to intracranial hypotension is predominantly dural, rather than leptomeningeal (discussed further in the section below).

causes of focal leptomeningeal enhancement

• Focal encephalitis or meningitis (e.g., tuberculous or fungal meningitis).
• Leptomeningeal carcinomatosis.
• Postictal hyperemia, following multiple seizures.(30273244)
• Infarction.
• Neurosarcoidosis.
• Post-operative or post-traumatic (delayed finding).
• Radiation therapy.

clues based on the quality of enhancement

• (1) Thin or streaky leptomeningeal enhancement:(31378868)
  • Bacterial or viral meningitis.
• (2) Thick, nodular, or lumpy contrast enhancement:(31378868)
  • Fungal or tuberculous meningitis.
  • Leptomeningeal carcinomatosis.
  • Neurosarcoidosis.

detection of leptomeningeal enhancement

• MRI is generally more sensitive than CT scan.  Most commonly, this is performed using a post-contrast T1 sequence.
• A post-contrast FLAIR sequence or a delayed post-contrast T1 sequence may improve sensitivity, but most MRI protocols don't include these.  Such sequences may be requested, if there is concern for leptomeningeal inflammation.

More on leptomeningeal enhancement from Radiopaedia: 🌊

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dural enhancement

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Dural enhancement (aka pachymeningeal enhancement, dura-arachnoid enhancement) doesn't hug the sulci and gyri of the brain.  Instead, this appears as enhancement adjacent to the skull and also involving the dural reflections (e.g., falx cerebri, tentorium cerebelli, falx cerebelli):

causes of dural enhancement

• Intracranial hypotension of any etiology (affects the dura, but strictly spares the leptomeninges).(26264063)
  • Following lumbar puncture (diffuse dural enhancement is seen in ~5% of patients).(26264063)
  • Benign intracranial hypotension.
  • Shunt or drain placement with overdrainage.
• Iatrogenic:
  • Status post craniotomy (may be limited to same hemisphere as procedure; often persists for years).(26264063)
  • Intrathecal chemotherapy.
• Meningitis (bacterial, viral, fungal, or tuberculous) – Typically causes leptomeningeal enhancement, more than dural enhancement.  Thus, when dural enhancement is seen, it is usually in combination with leptomeningeal enhancement.
• Neoplastic (dural metastases from breast or prostate carcinoma; primary CNS malignancy).
• Autoimmune (neurosarcoidosis;  rheumatoid meningitis; Vogt-Koyanagi-Harada; granulomatosis with polyangiitis).
• Other:
  • Chronic subdural hematoma.
  • CVT (cerebral venous thrombosis).
  • Subarachnoid hemorrhage.(23122257)  

More on dural enhancement from Radiopaedia: 🌊

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gyral enhancement

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Also known as cortical or gyriform enhancement, this involves enhancement of the superficial cortex (figure below).  Like leptomeningeal enhancement, this dives into the gyri – but unlike leptomeningeal enhancement, this is thicker.  

causes of gyral enhancement

• Vascular:
  • Recent ischemic stroke, especially following reperfusion.
  • Migraine headache.
  • Cerebral venous thrombosis with venous infarction.
  • PRES (posterior reversible encephalopathy syndrome).
• Postictal state.
• Infection:
  • Viral encephalitis (e.g., due to herpes simplex virus).
  • Tuberculosis.
• Cortical laminar necrosis due to medication toxicity (e.g., chemotherapy).
• Oncologic:
  • Glioblastoma or metastatic malignancy.
  • SMART syndrome (stroke migraine attacks after radiation therapy). 📖

More on gyral enhancement from Radiopaedia: 🌊

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solitary enhancing mass

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solitary enhancing mass (26046515)

• Metastasis:
  • Often rim-enhancing, located at the gray-white junction.
  • May be indistinguishable from a high-grade glioma.
• High-grade glioma:
  • Thick, irregular enhancement.
• Pyogenic abscess: 📖
  • Thick, smooth rim enhancement.
  • Mature abscess should have a necrotic core with restricted diffusion.
• Lymphoma: 📖
  • Isodense or hyperdense on CT scan.
  • Homogeneous enhancement in immunocompetent patients; may be rim-enhancing in immunocompromised patients.
  • Diffusion restriction is seen, but less intensely than with an abscess.
• Tumefactive multiple sclerosis: 📖
  • Variable enhancement patterns (classically an open ring, with the nonenhancing portion abutting the cortex).
• Subacute infarct:
  • Infarcts may enhance, beginning after one week and lasting a few months.
  • FLAIR abnormality matches enhancing mass (without surrounding vasogenic edema).
• Subacute intraparenchymal hemorrhage:
  • Complex heterogeneous enhancement, may have rim enhancement.
  • May have associated vasogenic edema.
  • Can be difficult to differentiate from a hemorrhagic mass.

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ring enhancing lesion(s)

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causes of ring enhancing lesion(s)

• Infection:
  • Bacterial abscess.
  • Cryptococcomas or other fungal abscesses.
  • Toxoplasmosis.
  • Tuberculoma.
  • Neurocysticercosis.
• Malignant:
  • Metastasis.
  • Glioblastoma.
  • Primary CNS lymphoma.
• Stroke:
  • Subacute infarct.
  • Resolving hematoma.
• Demyelination (may cause incomplete ring enhancement):
  • Tumefactive multiple sclerosis.
  • Balo concentric sclerosis.
  • ADEM (acute disseminated encephalomyelitis).
• Radiation necrosis.
• Postoperative change.
• Contusion.

radiographic features that may help differentiate among these

• Enhancing wall characteristics:
  • Thick, nodular wall enhancement suggests neoplasm.
  • Thin, consistent wall enhancement suggests abscess.
  • Incomplete ring enhancement opened towards cortex suggests demyelination.
  • Restricted diffusion of the wall suggests glioblastoma multiforme or demyelination.(Gaillard 2022)
• Lesion core:
  • Diffusion restriction is highly suggestive of abscess.
  • Lack of diffusion restriction may suggest malignancy with central necrosis.

More on ring enhancing lesions enhancement from Radiopaedia: 🌊

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U-fibers

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basics of U-fibers

• Subcortical U-fibers are short white-matter connections between adjacent gyri in the brain, located within the outermost rim of the white matter.  These are also known as “short association fibers” (figure above).(Riley et al. 2018)
• Biologically, U-fibers are somewhat unique:
  • U-fibers have very slow myelin turnover.
  • U-fibers are relatively protected from disease of small arterioles.  U-fibers receive dual perfusion, both from ascending branches of deep penetrating arterioles and descending branches of cortical arterioles.

diseases that spare the U-fibers initially

• Pathophysiology of disorders that initially spare U-fibers:
  • (1) Disorders involving myelin metabolism spare U-fibers initially.
  • (2) Disorders involving microvascular dysfunction tend to involve the deeper white matter.
• Radiological appearance:  Diseases that spare the U-fibers tend to involve the more central white matter, while sparing the most peripheral white matter.
• Differential diagnosis includes: (Riley et al. 2018)
  • Chronic, small-vessel ischemic white matter lesions (aka leukoaraiosis).
  • HIV encephalopathy.
  • Many toxic/metabolic encephalopathies (e.g., chemotherapy, radiation, delayed post-hypoxic leukoencephalopathy).
  • Many leukodystrophies and inborn errors of metabolism.

diseases that involve the U-fibers early/indiscriminately

• Pathophysiology:  Any disorder that doesn't involve myelin metabolism or the microvasculature may involve the white matter indiscriminately.  For example, demyelinating disorders that damage previously normal myelin and/or oligodendrocytes.
• Radiological appearance:  Diseases with early involvement of U-fibers may involve the white matter in a manner that extends out peripherally and touches the grey matter.
• Differential diagnosis includes: (Riley et al. 2018)
  • Multiple sclerosis (if there are juxtacortical lesions).
  • PML 📖 (progressive multifocal leukoencephalopathy).
  • ADEM (acute disseminated encephalomyelitis).
  • MS (multiple sclerosis).
  • PRES (posterior reversible encephalopathy syndrome).
  • CADASIL (Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy).

More on U-fibers from Radiopaedia: 🌊

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podcast

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• This is a book directed at generalists (e.g., intensivists) – not neuroradiologists.  For intensivists, the biggest imaging pitfall is hesitancy to call up the attending neuroradiologist to discuss imaging findings.  In situations where radiologic findings dictate immediate patient management, a discussion with a radiology expert can be extremely helpful.

Guide to emoji hyperlinks 

•  = Link to online calculator.
•  = Link to Medscape monograph about a drug.
•  = Link to IBCC section about a drug.
•  = Link to IBCC section covering that topic.
•  = Link to FOAMed site with related information.
• 📄 = Link to open-access journal article.
•  = Link to supplemental media.

Review of MRI sequences: