Patterns of Enhancement in the Brain

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

2. Mohamed Zaitoun
Assistant Lecturer-Diagnostic Radiology
Department , Zagazig University Hospitals
Egypt
FINR (Fellowship of Interventional
Neuroradiology)-Switzerland
zaitoun82@gmail.com

5. Knowing as much as
possible about your enemy
precedes successful battle
and learning about the
disease process precedes
successful management

6. Patterns of Enhancement in the Brain
1-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)

7. *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

8. -Several CNS regions don’t have a BBB and therefore
normally enhance :
a) Choroid plexus
b) Pituitary & pineal glands
c) 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)

9. Choroid plexus, 40 (T1+C)

10. Pituitary gland (T1+C)

11. Pituitary gland (T1+C)

12. Pineal gland (T1+C)

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

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

16. -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

17. 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.

18. 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

19. 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

20. 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

21. 2-Gyriform Enhancement (Intra-axial) :
-Causes :
1-Herpes encephalitis
2-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-PRES
4-Meningitis (may cause gyral enhancement in
addition to the more typical leptomeningeal
enhancement)

22. 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

23. 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)

24. 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

25. 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)

26. 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

27. -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

28. 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)

29. Nodular subcortical enhancement , metastases

30. 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)

31. 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

32. 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

33. 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

34. 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)

35. 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

36. 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

37. Ring enhancement in subacute basal ganglia infarct

38. 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

39. (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

40. 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)

41. (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

42. 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)

43. Ring enhancement in radiation necrosis

44. 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

45. -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

46. -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

47. 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 (*)

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

49. 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)

50. (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

51. 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

52. -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

53. 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

54. 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

55. (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

56. **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