Neurologic Imaging

Characteristic MRI Appearance

• Premature

  • Smooth cortical surface, lacking cortical folding

  • Gray-white matter (GWM) signal intensity reversal on T1W

• Cortex is hyperintense.

• Basal ganglia are hyperintense.

• Neonate: myelination of different structures depends on age.

• Myelination progresses from inferior to superior, central to peripheral, and posterior to anterior.

• T1 hyperintensity precedes T2 hypointensity in myelinated white matter (WM).

• Terminal zones of myelination: Symmetric T2 hyperintensity in the periatrial WM representing incompletely myelinated parietooccipital association fibers; a normal finding that can persist into the second and third decades of life

Cavum Septum Pellucidum

• Separates frontal horns of lateral ventricles (anterior to foramen of Monro)

• 80% of term nenonates; 15% of adults

• May dilate; rare cause of obstructive hydrocephalus

Cavum Vergae

• Posterior continuation of cavum septum pellucidum; never exists without cavum septum pellucidum.

Cavum Velum Interpositum

• Extension of quadrigeminal plate cistern to foramen of Monro

Segments and Branches of VAs ( Fig. 6.14 )

• Cervical segment (extradural)

  • Muscular branches

  • Spinal branches

  • Posterior meningeal artery

• Intracranial segment (intradural)

  • Anterior spinal artery (ASA)

  • Posterior inferior cerebellar artery (PICA)

• Basilar artery

  • Anterior inferior cerebellar artery (AICA)

  • Superior cerebellar artery (SCA)

  • Brainstem perforating arteries

  • Posterior cerebral artery (PCA)

Anterior Cerebral Artery (ACA) ( Fig. 6.16 )

Represents one of the two ICA terminal branches

• A1 segment:

  • Origin to ACOM

  • Medial lenticulostriates

• A2 segment:

  • From ACOM

  • Recurrent artery of Heubner

  • Frontal branches

• Terminal bifurcation

  • Pericallosal artery

  • Callosomarginal artery

Middle Cerebral Artery (MCA) (see Fig. 6.16 )

Represents the larger of the two terminal ICA branches

• M1 segment:

  • Origin to MCA bifurcation

  • Lateral lenticulostriates

• M2 segment:

  • Insular branches

• M3 segment:

  • Opercular branches

• M4 segment:

  • Cortical branches

Posterior Cerebral Artery (PCA)

• P1 segment:

  • Origin to PCOM

  • Posterior thalamoperforators

• P2 segment:

  • Distal to the PCOM

  • Thalamogeniculates

  • Posterior choroidal arteries

• Terminal cortical branches

Internal Carotid Artery (ICA) ( Fig. 6.17 )

Mnemonic: HOT Pepper :

• H ypoglossal artery: ICA (C1–C2) to basilar artery via hypoglossal canal

• O tic artery: petrous ICA to replace middle meningeal artery via middle ear (foramen spinosum may be absent)

• T rigeminal artery: cavernous ICA to basilar artery (most common), Neptune's trident sign on angiography

• P roatlantal intersegmental artery: cervical ICA to vertebrobasilar system

External Carotid Artery (ECA)

• Middle meningeal artery arises from ophthalmic artery

• Variation in order of branching

Circle of Willis

• Hypoplasia of PCOM

• Hypoplasia or absence of A1 segment

• Fetal PCA (originates from ICA) with atretic P1

• Hypoplastic ACOM

• Infundibulum of PCOM: take-off of PCOM from ICA is from apex of a triangular- or funnel-shaped origin measuring <3 mm; do not mistake for aneurysm

Meningeal Spaces

• Epidural space: potential space between dura mater (two layers) and bone

• Subdural space: space between dura and arachnoid

• Subarachnoid space: space between arachnoid and pia mater

B-Mode Imaging ( Fig. 6.21 )

Delineate common carotid artery (CCA), ECA, ICA, bulb

• Vessel wall thickness

  • >1.0 mm is abnormal.

  • All focal plaques are abnormal.

• Plaque characterization

  • Determine extent and location

  • Plaque texture

    • Homogeneous (dense fibrous connective tissue)

    • Heterogeneous (intraplaque hemorrhage: echogenic center; unstable)

    • Calcified (stable)

  • Plaque surface

    • Irregular surface may represent ulceration

• Evaluation of stenosis

  • Measure visible stenosis in transverse and longitudinal planes. Use Doppler measurements for degree of stenosis

  • Focal versus segmental stenosis

Doppler Imaging (Flow) ( Fig. 6.22 )

Doppler imaging displays velocity profile. Analysis of spectra:

• 1

  Analysis of waveform

  • Components of curve

    • Peak diastolic flow

    • Peak systolic flow

    • Peak broadness

    • Flow direction

  • Shape of curves

    • High-resistance vessels (e.g., ECA)

    • Low-resistance vessels (e.g., ICA)

    • Intermediate-resistance vessels (e.g., CCA)

  US DIFFERENTIATION BETWEEN ICA AND ECA

  Parameter	ICA	ECA
  Size	Large	Small
  Location	Posterior and lateral	Anterior and medial
  Branches	No	Yes
  Temporal tap	No pulsation	Pulsation
  Pulsatility	Not very pulsatile (low resistance)	Very pulsatile (high resistance)
  Waveform	Low resistance	High resistance
  	Flow in systole and diastole	Flow in systole only

  ECA , External carotid artery; ICA , internal carotid artery.

• 2

  Spectral broadening ( Fig. 6.23 )

  • When normal laminar blood flow is disturbed (by plaques and/or stenoses), blood has a wider range of velocities = spectral broadening.

  • Two ways to detect spectral broadening:

    • The spectral window is obliterated.

    • Automated determination of bandwidth = spread of maximum and minimum velocities

  

• 3

  Peak velocities ( Fig. 6.24 )

  • Flow velocities increase proportionally with the degree of a stenosis: flow of >250 cm/s indicates a >70% stenosis.

  • Carotid stent:

    • 50%–79% stenosis: >220 cm/s and ICA/CCA ratio ≥2.7

    • 80%–99% stenosis: >340 cm/s and ICA/CCA ratio ≥4.15

  

Color Doppler US

Color Doppler imaging (CDI) displays real-time velocity information in stationary soft tissues. The color assignment is arbitrary but conventionally displayed in the following manner:

• Red: toward transducer

• Blue: away from transducer

• Green: high-velocity flow

• Color saturation indicates speed.

  • Deep shades: slow flow

  • Light shades: fast flow

Pearls

• Perform CDI only with optimal gain and flow sensitivity settings.

  • Ideally the vessel lumen should be filled with color.

  • Color should not spill over to stationary tissues.

• Frame rates vary as a function of the area selected for CDI: the larger the area, the slower the frame rate.

• Laminar flow is disrupted at bifurcations.

• Do not equate color saturation with velocity: green-tagged flow in a vessel may represent abnormally high flow or simply a region in the vessel where flow is directed at a more acute angle relative to the transducer.

• When color flow is not present in the expected vessel, increase pulse Doppler frequency, decrease filters, and apply Doppler imaging within the vessel to detect blood flow in slow flow states such as pseudoocclusion or no flow in an occluded vessel.

• The angle of insonation should be within 0–60 degrees.

Location

• Basal ganglia (putamen > thalamus), 80%

• Pons, 10%

• Deep GM, 5%

• Cerebellum, 5%

Imaging Features

• Typical location of hemorrhage (basal ganglia) in hypertensive patient

• Mass effect from hemorrhage and edema may cause herniation of brain.

• If the patient survives, the hemorrhage heals and leaves a residual cavity that is best demonstrated by MRI.

Imaging Features ( Fig. 6.29 )

• Interpretation of conventional angiography

  • Number of aneurysms: multiple in 20%

  • Location, 90% in anterior circulation

    • Most commonly anterior communicating artery, ICA–PCA junction, and MCA bifurcation

    • Also basilar tip

  • Size

  • Relation to parent vessel

  • Presence and size of aneurysm neck

• CTA

  • >95% sensitive for aneurysms >2 mm

• Magnetic resonance angiography (MRA)

  • Usually combined with conventional MRI

  • Used to screen patients with risk factors (e.g., adult polycystic kidney disease [APKD])

  • Low sensitivity for aneurysms <4 mm

  • Need to verify presence of aneurysm by reviewing single-slice raw images

Complications

• Rupture

  • SAH

  • Parenchymal hematoma

  • Hydrocephalus

• Vasospasm

  • Occurs 4–5 days after rupture

  • Causes secondary infarctions

  • Leading cause of death/morbidity from rupture

• Mass effect

  • CN palsies (e.g., CN III palsy from ruptured posterior communicating artery aneurysm)

  • Headache

• Death, 30%

• Rebleeding

  • 50% rebleed within 6 months

  • 50% mortality

In the presence of multiple aneurysms, one may identify the bleeding aneurysm using the following criteria:

• Location of SAH or hematoma adjacent to or around bleeding aneurysm

  • Anterior communicating aneurysm → interhemispheric fissure

  • MCA bifurcation aneurysm → Sylvian fissure

  • ICA–posterior communicating artery junction aneurysm → suprasellar cistern

  • Vertebrobasilar aneurysm → fourth ventricle, prepontine cistern

• Largest aneurysm is the one most likely to bleed

• Most irregular aneurysm is the one most likely to bleed

• Extravasation of contrast (rarely seen)

• Vasospasm adjacent to bleeding aneurysm

Clinical Findings

• Mass effect (CN palsies, retroorbital pain)

• Hemorrhage

Imaging Features

• Large mass lesion with internal blood degradation products

• Signet sign: eccentric vessel lumen with surrounding thrombus

• Curvilinear peripheral calcification

• Ring enhancement: fibrous outer wall enhances after complete thrombosis

• Mass effect on adjacent parenchyma

• Slow erosion of bone

  • Sloping of sellar floor

  • Undercutting of anterior clinoid

  • Enlarged superior orbital fissure

Causes

• Bacterial endocarditis, intravenous drug abuse (IVDA), 80%

• Meningitis, 10%

• Septic thrombophlebitis, 10%

Imaging Features

• Aneurysm itself is rarely visualized by CT.

• Most often located peripherally and multiple (differential diagnosis [DDx]: tumor emboli from atrial myxoma)

• Intense enhancement adjacent to vessel

• Conventional angiography is the imaging study of choice.

Imaging Features

• Vertebrobasilar arteries are elongated, tortuous, and dilated.

• Tip of basilar artery may indent third ventricle.

• Aneurysm may be thrombosed.

  • CT: hyperdense

  • T1W: hyperintense

• Bizarre flow voids on MRI because of turbulent flow

Complications

• Brainstem infarction because of thrombosis

• Mass effect (CN palsies)

Imaging Features

• Elongated contrast collections extending beyond the vessel lumen

• MRA is a useful screening modality.

• CTA may be used for diagnosis and follow-up.

• Angiography is sometimes required for imaging of vascular detail (dissection site).

Causes

• Trauma

• Aneurysm (most common cause after trauma), 90%

• AVM/dural AV fistula

• Coagulopathy

• Extension of intraparenchymal hemorrhage (hypertension [HTN], tumor)

• Amyloid angiopathy

• Reversible cerebral vasoconstriction syndrome (RCVS)

• Idiopathic (e.g., perimesencephalic nonaneurysmal SAH)

• Spinal AVM

Imaging Features ( Fig. 6.30 )

• CT is the first imaging study of choice.

• Hyperdense CSF usually in basal cisterns, sylvian fissure (because of aneurysm location), and subarachnoid space

• Hematocrit effect in intraventricular hemorrhage

• MRI less sensitive than CT early on (deoxy-Hb and brain are isointense)

• MRI more sensitive than CT for detecting subacute (fluid-attenuated inversion recovery [FLAIR] bright)/chronic SAH (T2W/susceptibility dark)

Complications

• Hemorrhage-induced hydrocephalus is due to early ventricular obstruction and/or arachnoiditis.

• Vasospasm several days after SAH may lead to secondary infarctions.

• Leptomeningeal “superficial” siderosis (dark meninges on T2W): Fe deposition in meninges secondary to chronic recurrent SAH. The location of siderosis corresponds to the extent of central myelin. CNs I, II, and VIII are preferentially affected because these have peripheral myelin envelope. Other CNs have their transition points closer to the brainstem. If no cause is identified, MRI of the spine should be performed to exclude a chronically bleeding spinal neoplasm such as an ependymoma or a paraganglioma.

• Perimesencephalic SAH: angiography negative SAH; likely from venous bleed

Types

• Parenchymal, 80% (ICA and VA supply; congenital lesions)

• Dural, 10% (ECA supply; mostly acquired lesions)

• Mixed, 10%

Imaging Features ( Fig. 6.31 )

• MRI is imaging study of choice for detection of AVM; arteriography is superior for characterization and treatment planning.

• Serpiginous high and low signal (depending on flow rates) within feeding and draining vessels best seen by MRI/MRA.

• AVM replaces but does not displace brain tissue (i.e., mass effect is uncommon) unless complicated by hemorrhage and edema.

• Edema occurs only if there is recent hemorrhage or venous thrombosis with infarction.

• Flow-related aneurysm, 10%

• Adjacent parenchymal atrophy is common as a result of vascular steal and ischemia.

• Calcification, 25%

• Susceptibility artifacts on MRI if old hemorrhage is present.

Spetzler Criteria

• Higher score is associated with higher chance of hemorrhage

• Other factors associated with poorer prognosis/higher risk of hemorrhage:

  • Intranidal aneurysm

  • Aneurysm in the circle of Willis

  • Aneurysm in arterial feeder

  • Venous stasis

Complications

• Hemorrhage (parenchymal > SAH > intra­ventricular)

• Seizures

• Cumulative risk of hemorrhage is approximately 3% per year.

Imaging Features

• CT is often normal.

• MRI:

  • Foci of increased signal intensity on contrast-enhanced studies

  • T2W hypointense foci if hemorrhage has occurred

• Angiography is often normal but may show faint vascular stain.

Clinical Findings

• Seizures

• Focal deficits

• Headache secondary to occult hemorrhage

Imaging Features ( Fig. 6.33 )

• MRI is the imaging study of choice.

• Complex signal intensities because of blood products of varying age

• “Popcorn” lesion: bright lobulated center with complete black (hemosiderin) rim

• Always obtain susceptibility sequences to detect coexistent smaller lesions.

• May be calcified

• Variable contrast enhancement

• Angiography is usually normal.

• Multiple cavernous malformations may be acquired (e.g., after radiation) or hereditary (autosomal dominant [AD] inheritance, more common in Hispanics)

Imaging Features ( Fig. 6.34 )

• Angiography

  • Medusa head seen on venous phase (hallmark)

  • Dilated medullary veins draining into a large transcortical vein

• MRI

  • Medusa head or large transcortical vein best seen on spin-echo images or after administration of gadolinium (Gd)

  • Location in deep cerebellar WM or deep cerebral WM

  • Adjacent to the frontal horn (most common site)

• Hemorrhage best detectable with MR susceptibility sequences, 10%.

Imaging Features

• US

  • First-choice imaging modality

  • Sonolucent midline structure superior/posterior to third ventricle

  • Color Doppler US to exclude arachnoid/developmental cyst

• Angiography

  • Used to determine type and therapy

  • Endovascular embolization: therapy of choice

• MRI

  • Indicated to assess extent of brain damage that influences therapy

• Chest radiography

  • High-output CHF, large heart

Causes

• Cerebral infarction, 80%

  • Atherosclerosis-related occlusion of vessels, 45%

  • Small vessel disease, 15%

  • Cardioembolic, 15%

  • Other, 5%

• Intracranial hemorrhage, 15%

• Nontraumatic SAH, 5%

• Venous occlusion, 1%

Imaging Features

• Gray-scale imaging (B-scan) of carotid arteries

  • Evaluate plaque morphology/extent

  • Determine severity of stenosis (residual lumen)

  • Other features

    • Slim sign: collapse of ICA above stenosis

    • Collateral circulation

• Doppler imaging of carotid arteries

  • Severity of stenosis determined by measuring peak systolic velocity

    • 50%–70%: velocity 125–250 cm/s

    • 70%–90%: velocity 250–400 cm/s

    • >90%: velocity >400 cm/s

  • Stenoses >95% may result in decreased velocity (<25 cm/s)

  • 90% accuracy for >50% stenoses

  • Other measures used for quantifying stenoses

    • End-diastolic velocity (severe stenosis: >100 cm/s)

    • ICA/CCA peak systolic velocity ratio (severe stenosis: >4)

    • ICA/CCA peak end-diastolic velocity ratio

  • Innominate artery stenosis may cause right CCA/ICA parvus tardus

  • CCA occlusion may result in reversal of flow in ECA

• Color Doppler flow imaging of carotid arteries

  • High-grade stenosis with minimal flow (string sign in angiography) is detected more reliably than with conventional Doppler US.

• CT and MR angiography are used for confirmation of US diagnosis of carotid stenosis.

  • • On CTA, 1.0–1.5-mm residual lumen corresponds to 70%–90% stenosis.

    • To determine complete occlusion versus a string sign (near but not complete occlusion), delayed images must be obtained immediately after the initial contrast images.

    • At some institutions, carotid endarterectomy is performed on the basis of US and CTA/MRA if the results are concordant.

    • Pitfalls of US and MRA in the diagnosis of carotid stenosis:

      • Near occlusions (may be overdiagnosed as occluded)

      • Postendarterectomy (complex flow, clip artifacts)

      • Ulcerated plaques (suboptimal detection)

      • Tandem lesions (easily missed)

• Carotid arteriography (gold standard) is primarily used for:

  • Discordant MRA/CTA and US results

  • Postendarterectomy patient

  • Accurate evaluation of tandem lesions and collateral circulation

  • Evaluation of aortic arch (AA) and great vessels

Causes

• Large vessel occlusion, 50%

• Small vessel occlusion (lacunar infarcts), 20%

• Emboli

  • Cardiac, 15%

    • Arrhythmia, atrial fibrillation

    • Endocarditis

    • Atrial myxoma

    • Myocardial infarction (anterior infarction)

    • Left ventricular aneurysm

  • Noncardiac

    • Atherosclerosis

    • Fat, air embolism

• Vasculitis

  • SLE

  • Polyarteritis nodosa

• Other

  • Hypoperfusion (border zone or watershed infarcts)

  • Vasospasm: ruptured aneurysm, SAH

  • Hematologic abnormalities

    • Hypercoagulable states

    • Hb abnormalities (carbon monoxide [CO] poisoning, sickle cell)

  • Venous occlusion

  • Moyamoya disease

Imaging Features

• Angiographic signs of cerebral infarction

  • Vessel occlusion, 50%

  • Slow antegrade flow, delayed arterial emptying, 15%

  • Collateral filling, 20%

  • Nonperfused areas, 5%

  • Vascular blush (luxury perfusion), 20%

  • AV shunting, 10%

  • Mass effect, 40%

Cross-sectional imaging

• CT is the first study of choice in acute stroke in order to:

  • Exclude intracranial hemorrhage

  • Exclude underlying mass/AVM

• Most CT examinations are normal in early stroke.

• Early CT signs of cerebral infarction include:

  • Loss of gray–white interfaces (insular ribbon sign)

  • Sulcal effacement

  • Hyperdense clot in artery on noncontrast CT (dense MCA sign)

• Edema (maximum edema occurs 3–5 days after infarction)

  • Cytotoxic edema develops within 6 hours (detectable by MRI).

  • Vasogenic edema develops later (first detectable by CT at 12–24 hours).

• Characteristic differences between distributions of infarcts:

  • Embolic: periphery, wedge shaped

  • Hypoperfusion in watershed areas of ACA/MCA and MCA/PCA—border zone infarcts

  • Basal ganglia infarcts

  • Generalized cortical laminar necrosis

• Reperfusion hemorrhage is not uncommon after 48 hours.

  • MRI much more sensitive than CT in detection

  • Most hemorrhages are petechial or gyral.

  CT AND MRI APPEARANCE OF INFARCTS

  Factor	1st Day	1st Week	1st Month	>1 Month
  Stage	Acute	Early subacute	Late subacute	Chronic
  CT density a	Subtle decrease	Decrease	Hypodense	Hypodense
  MRI	T2W: edema	T2W: edema	Varied	T1W dark, T2W bright
  Mass effect	Mild	Maximum	Resolving	Encephalomalacia
  Hemorrhage	No	Most likely here	Variable	MRI detectable
  Enhancement	No	Yes; maximum at 2–3 weeks	Decreasing	No

  CT , Computed tomography; MRI , magnetic resonance image; T1W , T1-weighted; T2W , T2-weighted.

  a Caused by cytotoxic and vasogenic edema.

• Mass effect in acute infarction

  • Sulcal effacement

  • Ventricular compression

• Subacute infarcts

  • Hemorrhagic component, 40%

  • Gyral or patchy contrast enhancement (1–3 weeks)

  • GWM edema

• Chronic infarcts

  • Focal tissue loss: atrophy, porencephaly, cavitation, focal ventricular dilatation

  • Wallerian degeneration: distal axonal breakdown along white matter tracks

Pearls

• Cerebral infarcts cannot be excluded on the basis of a negative CT. MRI with diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) (see later discussion) should be performed immediately if an acute infarct is suspected.

• Contrast administration is reserved for clinical problem cases and should not be routinely given, particularly on the first examination.

• Luxury perfusion refers to hyperemia of an ischemic area. The increased blood flow is thought to be due to compensatory vasodilatation secondary to parenchymal lactic acidosis.

• Cerebral infarcts have a peripheral rim of viable but ischemic tissue (penumbra).

• Thrombotic and embolic infarcts occur in vascular distributions (i.e., MCA, ACA, PCA, etc.).

• MR perfusion/diffusion studies are imaging studies of choice in acute stroke.

  • DWI detects reduced diffusion coefficient in acute infarction, which is thought to reflect cytotoxic edema.

  • In patients with multiple T2W signal abnormalities from a variety of causes, DWI can identify those signal abnormalities that arise from acute infarction.

• 50% of patients with TIA have DWI abnormality.

Interpretation

• A typical infarct is DWI bright and ADC dark. Gliosis appears DWI bright because of T2 shine-through but is also bright on ADC.

• DWI is very sensitive for detecting disease (will pick up infarcts from about 30 min onward but is nonspecific and will also detect nonischemic disease).

• ADC is less sensitive than DWI, but dark signal is fairly specific for restricted diffusion, which usually means ischemia.

• Significance of a DWI-bright, ADC-dark lesion: this tissue will almost certainly go on to infarct and full necrosis. Rare instances of reversible lesions have been reported (venous thrombosis, seizures, hemiplegic migraine, hyperacute arterial thrombosis).

• EXP (exponential) is the map that “subtracts” the T2 effect. In equivocal cases, use EXP map as a problem solver (if it stays bright on the EXP map, then it is true restricted diffusion).

• MTT is highly sensitive for disturbances in perfusion but not good for prediction of later events. For example, an asymptomatic carotid occlusion would have a dramatically abnormal MTT, without the patient being distressed.

• CBV is a parameter that changes late in the ischemic cascade, and, usually, reduced CBV is also accompanied by restricted diffusion. Reduced CBV (and restricted diffusion) correlates well with tissue that goes on to infarction.

• CBF in the experimental setting can be used to predict the likelihood of brain tissue infarcting. In current clinical practice, a CBF abnormality exceeding the DWI abnormality (diffusion–perfusion mismatch) implies that there is brain at risk that has not infarcted yet. This brain at risk is the target of therapeutic interventions.

Technique

• Noncontrast CT is performed initially to exclude hemorrhage; an absolute contraindication to thrombolytic therapy. Large parenchymal hypodensity (> one-third of a vascular territory), typically indicating irreversible “core” of infarction, is a relative contraindication to thrombolysis.

• CTA/CTP imaging is performed on a multislice scanner, which enables acquisition of imaging data from entire vascular territories in <1 min.

• The initial CT scan is performed at 140 kV, 170 mA, pitch = “high quality” (3 : 1), and a table speed of 7.5 mm/s.

• Images are obtained from the skull base to the vertex. Slice thickness can be set at 2.5 mm, at 5 mm, or at both.

• Initial image review is in “real time,” directly at the CT console. The use of narrow window-width settings, with a center level of about 30 HU (width of 5–30 HU), facilitates the detection of early, subtle, ischemic changes contiguous with normal parenchyma.

• Blood volume CTP is performed without repositioning the patient.

• Approximately 90–120 mL of nonionic, isoosmolar contrast is used for CTA from the skull base to the vertex, with a 25-s scan delay. A longer delay may be needed for patients with compromised cardiac function and atrial fibrillation.

• Initial scan parameters are as per the noncontrast CT scan described earlier. A second phase of scanning is performed immediately, with minimal possible delay, from the AA to the skull base, with similar scan parameters except for an increase in the table speed to 15 mm/s. Major advantages of first scanning the intracranial circulation include (1) obtaining the most important data first, which can be reviewed during subsequent acquisition; and (2) allowing time for clearance of dense IV contrast from the subclavian, axillary, and other veins at the thoracic inlet, reducing streak artifact.

• On a >16-slice scanner, CTA may be performed from the vertex to the AA in one pass, with triggering of imaging when the contrast bolus reaches the arch (“smart prep”). This gets rid of the loss of contrast enhancement in the neck CTA usually seen with a two-stack protocol.

• Concerns related to radiation dose and variability in estimating infarct core have limited the utility of CTP in selecting acute stroke patients for IV thrombolysis or endovascular therapy.

Imaging Features

• MRI is the imaging study of choice.

• Small ovoid lesion (<1 cm): hyperintense on T2W and proton density–weighted (PDW) image.

• Location of lesions is very helpful in DDx:

  • Dilated perivascular or Virchow-Robin (VR) space

    • Typically located in the basal ganglia along the anterior commissure

    • Can be large (giant VR space), can cause mass effect, and can have surrounding gliosis

    • More elongated appearance on coronal images

Risk Factors

• Atherosclerosis

• Cardiac arrhythmias

• VA dissection

• Cocaine use

• Oral contraceptives (OCs)

Top of Basilar Artery Syndrome

• Oculomotor dysfunction

• Third nerve and vertical gaze palsies

• Hemiataxia

• Altered consciousness

Imaging Features

• Unlike anterior circulation infarction, the duration of symptoms before treatment, age of patient, and neurologic status at initiation of treatment do not predict the outcome of thrombolytic therapy.

• Basilar artery appears abnormally dense by CT.

• T2W hyperintensity is present in thalami, midbrain, pons, cerebellum, and occipital lobes.

• Absence of normal flow void in basilar artery and VA

• T1W with fat saturation may be useful, to look for associated dissection.

Causes

• Infectious vasculitis

  • Bacterial, viral, fungal, tuberculosis (TB), syphilis

  • Human immunodeficiency virus (HIV)-related

• Systemic vasculitis

  • Polyarteritis nodosa

  • Giant-cell arteritis/temporal arteritis

  • Takayasu arteritis

  • Kawasaki syndrome

  • Behçet disease

  • Collagen vascular diseases

  • Serum sickness

  • Allergic angiitis

• Granulomatous vasculitis

  • Sarcoidosis

  • Wegener granulomatosis

  • Granulomatous angiitis (primary and secondary)

• Drug-related vasculitis

  • Cocaine

  • Amphetamines

  • Ergots

  • Heroin

Imaging Features

• MRI

  • Most MRI findings are nonspecific.

  • T2W hyperintensities that progress rapidly are highly suggestive.

  • Infarctions

  • Hemorrhage

• Angiography

  • CTA may also show areas of focal narrowing, similar to catheter angiography.

  • Catheter angiography is the more definitive imaging study, but findings are often also nonspecific.

• Other imaging findings

  • Vessel occlusions

  • Stenoses

  • Aneurysms

Imaging Features

• “Puff of smoke” on angiography: numerous collaterals supplying ACA and MCA

• Stenosis or occlusion of supraclinoid ICA

• MRI: multiple tiny flow voids on T2W images, which are collaterals; engorged collaterals may produce FLAIR bright sulci (Ivy sign)

• Similar radiographic findings can be seen in (mnemonic: RAINS ):

  • R adiation vasculopathy

  • A therosclerosis

  • I diopathic (moyamoya)

  • N eurofibromatosis type 1

  • S ickle cell disease

Imaging Features

• Usually multiple areas of hemorrhage sparing the basal ganglia

• Foci of hemorrhage at corticomedullary junction

• MRI is the imaging study of choice (susceptibility sequences).

MRI Features

• Confluent T2 hyperintensities around periventricular WM, pons, and basal ganglia

• Predilection for the anterior temporal lobes

Causes

• Pregnancy/puerperium

• Dehydration (particularly in children)

• Infection (mastoiditis, otitis, meningitis)

• Tumors with dural invasion

• l -Asparaginase treatment

• Any hypercoagulable state

• Trauma

• OCs

• Blood dyscrasias and coagulopathies

Imaging Features ( Fig. 6.35 )

• General

  • CTV is the imaging method of choice, followed by magnetic resonance venography (MRV)

  • Location: superior sagittal sinus > transverse sinus > sigmoid sinus > cavernous sinus

• Primary (sinus occlusion)

  • Clot in sinus is hyperdense on noncontrast CT and hypodense on contrast-enhanced CT.

  • Dural enhancement of sinus margin: delta sign

  • MRI

    • Bright sinus on T1W and T2W (depending on stage)

    • Absence of flow void

  • Pearl: if bilateral thalamic infarcts or infarcts do not conform to an arterial territory, suspect venous thrombosis.

• Secondary (effects of venous infarction)

  • Subcortical infarctions, which may not follow arterial distribution

  • Corticomedullary hemorrhage is common.

Score

• Eye opening

  • Spontaneous = 4

  • To sound = 3

  • To pain = 2

  • None = 1

• Best motor response

  • Obeys command = 6

  • Localizes pain = 5

  • Normal flexion = 4

  • Abnormal flexion = 3

  • Extension = 2

  • None = 1

• Best verbal response

  • Oriented = 5

  • Confused = 4

  • Inappropriate words = 3

  • Incomprehensible = 2

  • None = 1

Types

• Arterial EDH, 90% (middle meningeal artery)

• Venous EDH, 10% (sinus laceration, meningeal vein)

  • Posterior fossa: transverse or sigmoid sinus laceration (common)

  • Parasagittal: tear of superior sagittal sinus

Large EDHs are neurosurgical emergencies. Small (<5-mm thick) EDHs adjacent to fractures are common and do not represent a clinical emergency. 95% of all EDHs are associated with fractures.

Imaging Features

• Arterial EDH

  • 95% are unilateral, temporoparietal

  • Biconvex, lenticular shape

  • Does not cross suture lines

  • May cross dural reflections (falx tentorium), in contradistinction to SDH

  • Commonly associated with skull fractures

  • Heterogeneity predicts rapid expansion of EDH, with areas of low density representing active bleeding.

• Venous EDH

  • More variable in shape (low-pressure bleed)

  • Often requires delayed imaging because of delayed onset of bleed after trauma

Imaging Features

• Morphology of hematoma

  • 95% supratentorial

  • Crescentic shape along brain surface

  • Crosses suture lines

  • Does not cross dural reflections (falx, tentorium)

  • MRI > CT particularly for:

    • Bilateral hematomas

    • Interhemispheric hematomas

    • Hematomas along tentorium

    • Subacute SDH

• Other imaging findings

  • Hematocrit level in subacute and early chronic hematomas

  • Mass effect is present if SDH is large.

• Acute SDH

  • Hyperdense or mixed density

• Subacute SDH (beyond 1 week)

  • May be isointense and difficult to detect on CT

  • Enhancing membrane and displaced cortical vessels (contrast administration is helpful)

• Chronic SDH (beyond several weeks)

  • Hypodense

  • Mixed density with rebleeding

  • Calcification, 1%

Imaging Features

• CSF density

• Does not extend into sulci

• Vessels cross through lesion.

• Main considerations in DDx:

  • Chronic SDH

  • Focal atrophy with widened subarachnoid space

Imaging Features ( Fig. 6.39 )

• Characteristic location of lesions:

  • Lobar GM/WM junction

  • Corpus callosum

  • Dorsolateral brainstem

• Initial CT is often normal.

• Petechial hemorrhage develops later.

• Multifocal T2W bright lesions

• May show restricted diffusion, especially in the corpus callosum

• Susceptibility-sensitive gradient-echo sequences are most sensitive in detecting hemorrhagic shear injuries (acute or chronic) and can be helpful to document the extent of parenchymal injury (medicolegal implications) and to assess long-term prognosis (cognitive function) for patient and family.

Imaging Features

• Characteristic location of lesions

  • Anterior temporal lobes, 50%

  • Inferior frontal lobes, 30%

  • Parasagittal hemisphere

  • Brainstem

• Lesions evolve with time; delayed hemorrhage in 20%

• Initial CT is often normal; later on, low-density lesions with or without blood in them develop.

• Late: encephalomalacia

Types

• Subfalcine herniation

• Transtentorial (uncal) herniation

  • Descending

  • Ascending

• Tonsillar herniation

Imaging Features ( Fig. 6.42 )

• Subfalcine herniation

  • Cingulate gyrus slips under free margin of falx cerebri.

  • Compression of ipsilateral ventricle

  • Entrapment and enlargement of contralateral ventricle

  • May result in ACA ischemia

• Descending transtentorial herniation (uncal) ( Fig. 6.43 )

  • Uncus/parahippocampal gyrus displaced medially over tentorium

  • Effacement of ipsilateral suprasellar cistern

  • Enlargement of ipsilateral cerebellopontine angle (CPA) cistern

  • Displaced midbrain impacts on contralateral tentorium.

    • Duret hemorrhage (anterior midbrain)

    • Kernohan notch (mass effect on peduncle)

  • PCA ischemia: occipital lobe, thalami, midbrain

  

• Ascending transtentorial herniation

  • Posterior fossa mass (i.e., hemorrhage) pushes cerebellum up through incisura.

  • Loss of quadrigeminal cistern

• Tonsillar herniation

  • Cerebellar tonsils pushed inferiorly

Imaging Features

• Findings develop 24–48 hours after injury.

• Effacement of sulci and basilar cisterns

  • Hint: the sulci near the vertex should always be present no matter how young the patient is, unless there is edema.

• Loss of perimesencephalic cisterns (hallmark)

• Loss of GM/WM interface (cerebral edema)

• White cerebellum sign: sparing of brainstem and cerebellum in comparison with the cerebral hemispheres

• Pseudosubarachnoid hemorrhage sign: apparent hyperdensity in the sulci and basal cisterns due to diffuse hypoattenuation of the brain parenchyma

Underlying Causes

• Spontaneous or with minimal trauma (strain, sports)

• Trauma

• HTN

• Vasculopathy (FMD, Marfan syndrome)

• Migraine headache

• Drug abuse

Imaging Features

• CTA is preferred first study of choice—see intimal flap and caliber change

• MRI/MRA can also be performed.

  • T1W bright hematoma in vessel wall (sequence: T1W with fat saturation): must be interpreted in conjunction with MRA

  • MRA string sign

• Conventional angiography may establish the diagnosis and fully elucidate abnormal flow patterns.

• Long-segment fusiform narrowing of affected artery

Complications

• Thrombosis

• Emboli and infarction

• Intramural hemorrhage

• False aneurysm

Types

• Traumatic CCF (high flow)

• Spontaneous CCF

  • Rupture of aneurysm in its cavernous segment (less common; high flow)

  • Dural fistula (AVM) of the cavernous sinus (low flow); usually associated with venous thrombosis in older patients

Imaging Features

• Enlargement of ipsilateral cavernous sinus

• Enlargement of superior ophthalmic vein

• Proptosis

• Enlargement of extraocular muscles

• Angiographic embolization with detachable balloons (traumatic fistulas)

Pearl

• Glial cells have high potential for abnormal growth. There are three types of glial cells: astrocytes (astrocytoma), oligodendrocytes (oligodendroglioma), and ependymal cells (ependymoma).

Classification

• Diffuse astrocytoma, World Health Organization (WHO) grade II

• Anaplastic astrocytoma, WHO grade III

• Glioblastoma multiforme, WHO grade IV

• Diffuse midline glioma, WHO grade IV

Imaging Features

• Focal or diffuse mass lesions

• Calcification, 20%

• Hemorrhage and extensive edema are rare.

• Mild enhancement

Imaging Features

• Heterogeneous mass

• Calcification uncommon

• Edema common

• Enhancement (reflects blood-brain barrier disruption [BBBD])

Imaging Features

• Usually heterogeneous low-density mass (on CT)

• Strong contrast enhancement

• Hemorrhage, necrosis common

• Calcification is uncommon.

• Extensive vasogenic edema and mass effect

• Bihemispheric spread via corpus callosum or commissures (butterfly lesion)

• High-grade gliomas located peripherally can have a broad dural base and a dural tail, mimicking an extraaxial lesion.

• CSF seeding: leptomeningeal drop metastases

Imaging Features

• Gliomatosis predominantly causes expansion of WM but may also involve deep gray nuclei and cortex.

• Usually nonenhancing lesions

• Late in disease, small foci of enhancement become visible.

• Leptomeningeal gliomatosis can mimic meningeal carcinomatosis or leptomeningeal spread of primary CNS tumors and cause marked enhancement.

• Important considerations in DDx for gliomatosis include:

  • Lymphomatosis cerebri

  • Multicentric glioma

  • Viral encephalitis

  • Vasculitis

  • Extensive active demyelinating disease such as acute disseminated encephalomyelitis (ADEM)

Clinical Findings

• CN VI and VII neuropathy

• Long tract signs

• Hydrocephalus

Imaging Features

• Enlargement of brainstem

• Posterior displacement of fourth ventricle (floor of the fourth ventricle should be in the middle of the Twining line: sella tuberculum – torcular)

• Encasement of basilar artery

• Cystic portions uncommon

• Hydrocephalus, 30%

• Enhancement occurs in 50% and is usually patchy and variable.

• Exophytic extension into basilar cisterns

• Brainstem encephalitis or demyelinating disease may mimic a diffuse midline glioma.

Imaging Features

• Cerebellar tumors are usually cystic and have an intensely enhancing mural nodule.

• Calcification, 10%

• Optic chiasm/hypothalamic tumors are solidly enhancing

• Most in brainstem show little enhancement.

• Focal tumors localized to the tectal plate are termed tectal gliomas and constitute a distinct subset of brainstem gliomas. Because these tumors have good long-term prognosis and are located deep, they are usually followed without biopsy and with serial imaging to document stability. If a lesion extends beyond the tectum but is still confined to the midbrain, it is referred to as a peritectal tumor and carries a worse prognosis than that for purely tectal lesions. Peritectal tumors may be difficult to differentiate from pineal region tumors.

Imaging Features

• Cortically based, often meningeal attachment with associated dural thickening and enhancement +/− calvarial remodeling

• Homogeneously enhancing

• May have cystic component with an enhancing nodule

Imaging Features

• Commonly involve cortex

• Typically hypodense mass lesions

• Cysts are common.

• Large nodular, clumpy calcifications are typical, 80%

• Hemorrhage and necrosis are uncommon.

• Enhancement depends on degree of histologic differentiation.

• Pressure erosion of calvaria occurs occasionally.