C.N.S.Patterns of Enhancement in the Brain

Mohamed Zaitoun

Assistant Lecturer-Diagnostic Radiology Department , Zagazig University Hospitals

EgyptFINR (Fellowship of Interventional

Neuroradiology)-Switzerlandzaitoun82@gmail.com

Knowing as much as possible about your enemy precedes successful battle

and learning about the disease process precedes successful management

Patterns of Enhancement in the Brain1-Periventricular Enhancement (Intra-axial)2-Gyriform Enhancement (Intra-axial)3-Nodular Subcortical Enhancement (Intra-axial)4-Ring Enhancement (Intra-axial)5-Pachymeningeal (Dural) Enhancement (Extra-

axial)6-Leptomeningeal (Pia-arachnoid) Enhancement

(Extra-axial)

*Blood Brain Barrier (BBB) & Enhancement :-Micro or macro disruption of the BBB produces a

parenchymal enhancement after contrast administration, which may be secondary to infection, inflammation, neoplasm, trauma and vascular etiologies

-The BBB is formed by astrocyte foot processes of brain capillary endothelial cells & prevents direct communication between the systemic capillaries & the protected extracellular fluid of the brain

-Several CNS regions don’t have a BBB and therefore normally enhance :

a) Choroid plexusb) Pituitary & pineal glandsc) Tuber cinereum (controls circadian rhythm, located in the

inferior hypothalamus)d) Area postrema (controls vomiting, located at inferior

aspect of the 4th ventricle)-The dura also lacks a BBB , but doesn’t normally enhance-Intracranial enhancement may be intra or extra-axial,

extra-axial structures that may enhance in pathologic conditions include the dura (pachymeninges) & arachnoid (leptomeninges)

Choroid plexus, 40 (T1+C)

Pituitary gland (T1+C)

Pituitary gland (T1+C)

Pineal gland (T1+C)

Tuber cinereum (a) T1, (b) T1+C

T2 shows the approximate location of the circumventricular area postrema (yellow circle) in the dorsal medulla adjacent

-Vascular enhancement is due to a localized increase in blood flow, which may be secondary to vasodilatation, hyperemia, neovascularity or arteriovenous shunting

-On CT, the arterial phase of contrast injection (for instance CTA) mostly shows intravascular enhancement, parenchymal enhancement, including the dural folds of the falx and tentorium, is best seen several minutes after the initial contrast bolus

-On MRI, routine contrast-enhanced sequences are obtained in the parenchymal phase, several minutes after injection, most intracranial vascular MRI imaging is performed with a non-contrast time of flight (TOF) technique

1-Periventricular Enhancement (Intra-axial) :-Enhancement of the subependymal surface can

be either neoplastic, infections or demyelinating in etiology

-Causes :1-Primary CNS lymphoma (presentations include

periventricular enhancement, solitary brain mass or multiple brain masses)

2-Infectious ependymitis (most commonly by CMV)3-Primary glial tumor (high grade astrocytoma)4-M.S.

Periventricular pattern, diagram illustrates thick periventricular enhancement as shown around the right lateral ventricle, this enhancement pattern is usually neoplastic and is most commonly seen in primary CNS lymphoma & high-grade astrocytoma, thin periventricular enhancement as shown around the left lateral ventricle is usually infectious

Thick periventricular enhancement in primary CNS lymphoma in an adult patient with AIDS. , (a) NECT shows a thick rind of periventricular hyperattenuation with surrounding vasogenic edema (b) CT+C shows abnormal enhancement around both lateral ventricles this (rind) is much thicker around the right lateral ventricle and involves the same areas that were hyperattenuating before contrast material administration

Thin periventricular enhancement in cytomegalovirus ependymitis , T1+C show abnormal enhancement completely surrounding both lateral ventricles , the enhancement is thin and very uniform , CMV causes an inflammation of the ventricular lining and produces ependymitis

2-Gyriform Enhancement (Intra-axial) :-Causes :1-Herpes encephalitis2-Subacute Infarct (can show gyriform

enhancement, lasting 6 days to 6 weeks after the initial ischemic event, in contrast to gyriform enhancement of subacute infarct, an acute infarct may show vascular enhancement due to reactive collateral vasodilatation and resultant hyperemia

3-PRES4-Meningitis (may cause gyral enhancement in

addition to the more typical leptomeningeal enhancement)

Cortical gyral enhancement , Diagram illustrates gyral enhancement that is localized to the superficial gray matter of the cerebral cortex , there is no enhancement of the arachnoid and none in the subarachnoid space or sulci

T1+C in a case of herpes encephalitis shows multifocal intra-axial curvilinear , cortical gyri-form enhancement that involves both temporal lobes , the enhancement is most prominent on the right but is also seen in the left insular region (arrows) as well as in the medial frontal lobes and cingulate gyrus (arrowhead)

Cortical gyral enhancement in embolic cerebral infarction , (a) NECT shows the sulci in the right hemisphere are normally prominent , on the left , the parietal sulci are effaced within a wedge-shaped region of abnormal hypoattenuation , the gyral surface is actually slightly hyperattenuating due to reperfusion injury with secondary petechial hemorrhage in the infarcted cortex , (b) CT+C shows cortical gyral enhancement , the same endothelial damage that allows red cells to extravasate also permits contrast material to escape the vascular lumen and enter the brain parenchyma

Cortical gyral enhancement in subacute thrombotic cerebral infarction , CT+C shows enhancement that is limited to the opercular surfaces , insula and caudate nucleus head (all of which are gray matter)

3-Nodular Subcortical Enhancement (Intra-axial) :-Nodular intra-axial enhancement is most commonly due to

metastatic disease-Hematogenously disseminated metastatic disease is small

(<2 cm) circumscribed lesions, commonly found subcortical, in or near the gray matter-white matter (corticomedullary) junction, whereas primary tumors are usually deeper

-Metastatic disease usually travels into the brain through the arteries and less commonly via the venous system

-CNS metastases are distributed by blood flow and the majority are supratentorial in the cerebral hemispheres, most often in the territory of the middle cerebral artery

-Venous dissemination of metastases (e.g. pelvic malignancy spread via the Batson prevertebral venous plexus) leads to posterior fossa (cerebellum & brainstem) disease by transit through the retroclival venous plexus

-Edema is almost always present with metastatic disease of the gray-white junction, although slightly more distal cortical metastases mayn’t show any edema and may be detectable only on the post-contrast images

 

Subcortical nodular enhancement , Diagram illustrates nodular lesions near the gray matter-white matter junction and one near the deep gray matter , this pattern is typical for metastatic cancer and clot emboli , because of their typical subcortical location , metastases often manifest with cortical symptoms or seizures while the lesions are small (often <1 cm in diameter)

Nodular subcortical enhancement , metastases

4-Ring Enhancement (Intra-axial) :-The two most common causes are high-grade

neoplasm & cerebral abscess-The mnemonic (MAGIC DR) :1-Metastases (hematogenous metastases are

typically at the subcortical gray-white junction, metastases are often multiple, but smaller lesions mayn’t be ring-enhancing

2-Abscess (the key finding is reduced diffusivity, bright on DWI & dark on ADC, caused by high viscosity of central necrosis & a characteristic smooth, hypointense rim on T2)

Subcortical nodular enhancement in metastatic breast cancer , T1+C shows multiple ring-enhancing lesions from necrosis of the metastases , the majority of these lesions are near the cortex or deep gray matter with most being at the gray matter-white matter junction , this appearance is similar to those of septic emboli and abscesses which indicates the need for good clinical correlation

Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess , Diagram illustrates a thin (<10 mm) rim of enhancement which is usually very smooth along the inner margin , this pattern is characteristic of an abscess , the lesion is surrounded by a crown of vasogenic edema spreading into the white matter

Smooth ring-enhancing pattern in late cerebritis and subsequent cerebral abscess , (a) T1+C shows the inner wall of the ring-enhancing lesion is smoother than the slightly irregular outer wall , this appearance reflects an earlier stage in the organization of the infection , as it makes the transition from cerebritis to abscess , since a more organized abscess will appear smoother , (b) CT+C shows a sharply marginated ringed lesion with surrounding perilesional vasogenic edema , (c) DWI shows the lesion has markedly restricted diffusion (hyperintensity) due to the viscous pus and necrotic brain tissue in the abscess core

3-Glioma (high grade tumors such as GBM typically have a thick & irregular wall), MRS will be abnormal outside the margin of an enhancing high grade glial neoplasm secondary to nonenhancing infiltrative tumor, this is in contrast to a demyelinating lesion, abscess and metastases, where the spectral pattern returns to normal at the margin of the lesion, MRI perfusion shows elevated perfusion in a high grade glioma

4-Infarct (although subacute cortical infarcts often show gyral enhancement, ring enhancement can be seen in subacute basal ganglia infarcts, in contrast to neoplasm & infection, a subacute infarct doesn’t have significant mass effect)

Necrotic ring pattern of high-grade neoplasms , (a) Diagram illustrates a lesion with an enhanced rim that is very thick medially , the ring is thicker and more irregular than that seen in a typical abscess , the lesion is surrounded by a crown of vasogenic edema spreading into the white matter , (b) GBM , T1+C shows the irregular heterogeneous ring-enhancing mass , the ring has a characteristically undulating or wavy margin and its inner aspect is shaggy and irregular

GBM , T1+C shows a mass with a complex appearance , the outer cortical region of the tumor (*) has a thick irregular rim with a shaggy inner margin (an appearance that is more typical of a glioblastoma multiforme) , the relatively smooth and thin deep inner margin mimics the thin reactive rim of an abscess wall

Ring enhancement in subacute basal ganglia infarct

5-Contusion (both traumatic & nontraumatic intraparenchymal hemorrhage can show ring enhancement in the subacute to chronic stage)

6-Demyelinating disease (the key finding in ring-enhancing demyelinating disease is lack of significant mass effect, the “ring” of enhancement is often incomplete & “C” shaped), MS is the most common demyelinating disease, enhancement suggests active disease, although the typical finding is an incomplete rim of enhancement, tumefactive demyelinating disease can look identical to a high-grade tumor

(a) Day 1 , NECT shows focal hyperdensity in the left frontal lobe representing a contusion , (b) After 10 days , NECT shows evolution of the left frontal contusion which is now hypodense , (b) CT+C shows ring enhancement

Open ring pattern , Diagram illustrates a lesion with an incomplete rim (only part of the rim enhances) , this appearance may be seen in multiple sclerosis (without mass effect as in this drawing) , tumefactive demyelination (with mass effect)

(a) T1+C shows two rimmed lesions , neither has a completely circumferential rim of enhancement (arrows) , the left frontal lesion has a more conspicuous open ring sign , note the absence of surrounding vasogenic edema , another potential differential feature to distinguish demyelination from both abscess and neoplasm , (b) T2 shows the two homogeneous , hyperintense lesions and the conspicuous absence of vasogenic edema

7-Radiation Necrosis (may look identical to a high-grade tumor, on perfusion, cerebral blood volume is generally low in radiation necrosis and typically increased in a high grade glioma)

Ring enhancement in radiation necrosis

5-Pachymeningeal (Dural) Enhancement (Extra-axial) :

-The pachymeninges (pachy means thick, a thick-skinned elephant is a pachyderm, refers to the dura matter)

-In addition to surrounding the surface of the brain, the dura forms several reflections, including the falx, tentorium & cavernous sinus

-The dura doesn’t have a BBB, although contrast molecules normally diffuse into the dura on enhanced CT or MRI, dural enhancement is never visualized on CT & is only visualized on MRI in pathologic situations

-Dural enhancement isn’t seen on CT because both the skull & adjacent enhancing dura appear white

-Enhancement of normal dura isn’t visible on MRI because MRI visualization of enhancement requires both water protons & gadolinium, although gadolinium is present in the dura, there are normally very few water protons, however, dural pathology often causes dural edema, which provides enough water protons to make the gadolinium visible, therefore, dural enhancement on MRI is an indication of edema rather than BBB breakdown

-Causes :a) Intracranial hypotension :-Prolonged decrease in CSF pressure can lead to

vasogenic edema in the dura-Clinically presents as a postural headache

exacerbated by standing upright-May be idiopathic or secondary to CSF leak from

surgery or lumbar puncture-Imaging shows thick linear dural enhancement,

enlargement of the pituitary gland and sagging of the cerebellar tonsils, there may be also subdural hemorrhage due to traction effect on the cerebral veins

Dura-arachnoid pachymeningeal enhancement , (a) Diagram shows dura-arachnoid enhancement which occurs adjacent to the inner table of the skull , in the falx within the interhemispheric fissure and also in the tentorium between the cerebellum , vermis and occipital lobes , pure dural enhancement without pial or subarachnoid involvement , will not fill in the sulci or basilar cisterns. (b) Postoperative T1+C of a patient in whom a shunt catheter had been placed in the high right parietal region (arrow) demonstrates diffuse and relatively thin dura-arachnoid enhancement along the inner table of the skull and in the dural reflections of the falx and tentorium (arrowheads) , there are bilateral subdural fluid collections , larger on the right (*)

Diffuse dural enhancement in intracranial hypotension , T1+C show diffuse dural enhancement (arrows)

b) Postoperative : dural enhancement may be seen postoperatively

c) Post lumbar puncture : diffuse dural enhancement is occasionally seen after routine lumbar puncture

d) Meningeal neoplasm : such as meningioma, can produce a focal area of dural enhancement called a dural tail due to reactive changes in the dura, metastatic disease to the dura most commonly breast cancer in a female and prostate cancer in a male, can cause irregular dural enhancement

e) Granulomatous disease : including sarcoidosis, TB & fungal disease, can produce dural enhancement, typically of the basal meninges (meninges of the skull base)

(a) Diagram illustrates the thin , relatively curvilinear enhancement that extends from the edge of a meningioma , most of this enhancement is caused by vasocongestion and edema , rather than neoplastic infiltration , the bulk of the neoplastic tissue is in the hemispheric extraaxial mass , nonetheless , the dural tail must be carefully evaluated at surgery to avoid leaving neoplastic tissue behind , (b) T1+C shows  a large extraaxial enhancing mass , the dural tail (arrows) extends several centimeters from the smooth edge of the densely enhancing hemispheric mass , most of this dural tail enhancement is caused by reactive changes in the dura mate

6-Leptomeningeal (Pia-arachnoid) Enhancement (Extra-axial) :

-The leptomeninges (lepto means thin or narrow) include the pia & arachnoid

-Leptomeningeal enhancement follows the undulating contours of the sulci as it includes enhancement of both the subarachnoid space and the pial surface of the brain

-Causes :1-Meningitis :-Bacterial, viral or fungal is the primary consideration

when leptomeningeal enhancement is seen-Leptomeningeal enhancement in meningitis is

caused by BBB breakdown due to inflammation or infection

-Fine linear enhancement suggests bacterial or viral meningitis

-Thicker nodular enhancement suggests fungal meningitis

2-Leptomeningeal carcinomatosis :-Also called carcinomatous meningitis -Is spread of neoplasm into the subarachnoid

space which may be due to primary brain tumor or metastatic disease

-CNS neoplasms known to cause leptomeningeal carcinomatosis include medulloblastoma, oligodendroglioma, choroid plexus tumor, lymphoma, ependymoma, glioblastoma & germinoma (MOCLEGG)

-metastatic tumors known to cause carcinomatosis include lymphoma & breast cancer

3-Viral encephalitis :-May produce cranial nerve enhancement within

the subarachnoid space

Pia-arachnoid leptomeningeal enhancement , Diagram illustrates the enhancement pattern which follows the pial surface of the brain and fills the subarachnoid spaces of the sulci and cisterns

(a) CT+C , (b) T1+C in a case of carcinomatous meningitis show pia-arachnoid enhancement along the surface of the brain and extending into the subarachnoid spaces between the cerebellar folia

**N.B. :-The D.D. of FLAIR hyperintensity in the subarachnoid

space overlaps with the differential for leptomeningeal enhancement, subarachnoid FLAIR hyperintensity may be due to :

1-Meningitis & leptomeningeal carcinomatosis : both have increased subarachnoid FALIR signal & leptomeningeal enhancement

2-SAH : manifests as increased subarachnoid FLAIR signal without leptomeningeal enhancement, blooming artifact on GRE or SWI from blood products will help differentiate SAH from carcinomatosis