This document discusses white matter and Virchow-Robin spaces as seen on MRI. It defines white matter as mostly glial cells and myelinated axons connecting brain regions. Virchow-Robin spaces normally surround blood vessels but may enlarge with age. Three characteristic enlarged types are described along lenticulostriate arteries, perforating medullary arteries, and in the midbrain. Differential diagnoses of enlarged Virchow-Robin spaces include lacunar infarctions, cystic leukomalacia, multiple sclerosis lesions, and others. Normal aging changes like punctate white matter lesions and mild atrophy are also reviewed.

1. By
Ibrahim Abd El Rassoul

2. White matter
is one of the two components of the
central nervous system and consists
mostly of glial cells and myelinated axons
that transmit signals from one region of
the cerebrum to another and between the
cerebrum and lower brain centers

3. Anatomy of white matter
 Assosciation fibres
connect centers of the same cerebral
hemisphere
it is divided into short and long fibers
 Projection fibres connect centers of
cerebral hemisphere with the lower centers
it is divided into ascending & descending
tracts

5. Commissural fibres
connect centers from cerebral hemisphere
with other hemisphere
1- corpus callosum
2-Anterior commissure
3-Posterior commissure
4-Hippocambal commissre
5-Habenular commissure

7. Virchow-Robin (VR) spaces

8. Virchow-Robin (VR) spaces
 Virchow-Robin (VR) spaces surround the
walls of vessels (perivascular) as they course
from the subarachnoid space through the
brain parenchyma.
 Small VR spaces appear in all age groups.
With advancing age, VR spaces are found
with increasing frequency and larger
apparent sizes.

9. Virchow-Robin (VR) spaces

10. Virchow-Robin (VR) spaces
 The signal intensity of VR spaces is identical
to that of cerebrospinal fluid with all
magnetic resonance imaging sequences.
 Occasionally, VR spaces have an atypical
appearance. They may become very large,
predominantly involve one hemisphere,
assume bizarre configurations, and even
cause mass effect.

11. Virchow-Robin (VR) spaces
 Knowledge of the signal intensity
characteristics and locations of VR spaces
helps differentiate them from various
pathologic conditions, including lacunar
infarctions, cystic periventricular
leukomalacia, multiple sclerosis,
cryptococcosis, mucopolysaccharidoses,
cystic neoplasms, neurocysticercosis,
arachnoid cysts, and neuroepithelial cysts.

12. Pathophysiology
The mechanisms underlying expanding VR
spaces are still unknown. Different theories have
been suggested:
1- Vascular ectasia:
Spiral elongation of blood vessels and brain
atrophy resulting in an extensive network of
tunnels filled with extracellular water

13. 2-Abnormality of arterial wall permeability:
due to segmental necrotizing angiitis of the
arteries.
3- Increased CSF pulsations:
expanding VR spaces resulting from
disturbance of the drainage route of interstitial
fluid due to cerebrospinal fluid (CSF)
circulation in the cistern .

14. 4- gradual leaking of the interstitial fluid
from the intracellular compartment to the pial
space around the metarteriole through the
fenestrae in the brain parenchyma
5- fibrosis and obstruction of VR spaces
along the length of arteries and consequent
impedance of fluid flow

16. Virchow robin spaces
Visually, the signal intensities of the VR
spaces are identical to those of CSF with all
pulse sequences.
VR spaces do not enhance with contrast
material.
In patients with small to moderate
dilatations of the VR spaces, the surrounding
brain parenchyma has normal signal
intensity

17. Virchow-Robin (VR) spaces
 VR spaces are mostly seen as well-defined
oval, rounded, or tubular structures. They
have smooth margins, commonly appear
bilaterally.
 Small VR spaces (<2 mm) appear in all age
groups. With advancing age, VR spaces are
found with increasing frequency and larger
apparent size (>2 mm)

19. Dilated VR spaces typically
occur in three characteristic
locations

20. Type I VR spaces
 Type I VR spaces
Appear along the
lenticulostriate arteries
entering the basal ganglia
through the anterior
perforated substance.

21. Type I VR spaces

22. Type II VR spaces
 Type II VR spaces are found along the paths of the
perforating medullary arteries over the high
convexities and extend into the white matter.

23. Type II dilated VR spaces

24. Type III VR spaces
 Type III VR spaces appear in the midbrain.

25. Type III VR

26. Type I VR
spaces
Type II VR
spaces
Type III VR
spaces

28. Virchow-Robin (VR) spaces
 Occasionally, VR spaces appear markedly
enlarged, cause mass effect, and assume
bizarre cystic configurations may cause
hydrocephalus by direct compression of the
third ventricle or the sylvian aqueduct
 May be misinterpreted as other pathologic
processes, most often a cystic neoplasm.

29. ENLARGED
TYPE III VR
SPACES

32. Lacunar Infarctions
 Lacunar infarctions are small infarctions
lying in deeper noncortical parts of the
cerebrum and brainstem. Sites of
predilection are the basal ganglia, thalamus,
internal and external capsule, ventral pons,
and periventricular white matter.

33. VR SPACES LACUNAR INFARCTION
*upper two-
thirds of the
anterior
perforated
substance and
basal ganglia
*the inferior
third of the
anterior
perforated
substance and
basal ganglia

34. Lacunar infarction
 Lacunar infarctions tend to be:
*larger than VR spaces
*exceed 5 mm,
*not symmetric,
*wedge-shaped holes
 Acute infarction ---restricted on diffusion WI with
corresponding low signal intensity on the apparent
diffusion coefficient map, enhancement is variable.

35. Lacunar infarction
 Chronic lacunar infarction: FLAIR images, a
hyperintense lesion or a lesion with a
hypointense center and a hyperintense rim
reflecting gliosis is seen. Diffusion-weighted
images are normal. Enhancement may
persist up to 8 weeks.

36. Acute lacunar infarction

37. Chronic lacunar infarction

38. Acute and chronic lacunar infarctions

40. Cystic Periventricular
leukomalacia
 Periventricular leukomalacia, usually seen in
premature infants, resulting from a pre- or
perinatal hypoxic-ischemic event
 DD from VR spaces---
*Corpus callosal thinning,
*Sparing of the overlying cortical structures,
*Surrounding gliosis, (FLAIR images)

41. Cystic periventricular leukomalacia

43. Multiple Sclerosis
 MS is a demyelinating disease CCC by lesions in the
periventricular and juxtacortical white matter
correspond to the location of type II VR spaces.
 DD from VR spaces---
 In the acute stage, MS are isointense or hypointense
on T1WI.
 In the chronic phase hypointense center with a
mildly hyperintense rim on T1WI.
Hyperintense in T2-weighted and FLAIR images
Enhancement (active inflammation )

44. Multiple sclerosis

47. Cryptococcosis
 Cryptococcosis is an opportunistic fungal infection
caused by Cryptococcus neoformans.
 Infection usually starts as meningitis.
 As the infection spreads along the VR spaces, they may
become distended with mucoid, gelatinous material.
 DD from VR spaces:
Punctate hyperintense areas seen in the basal ganglia,
thalami, and midbrain on T2 and FLAIR,

48. Cryptococcosis

50. Mucopolysaccharidoses
 The mucopolysaccharidoses are inherited disorders of
metabolism characterized by enzyme deficiency and
inability to break down glycosaminoglycan (GAG)
 the VR spaces are dilated by accumulated GAG
 DD from VR spaces:
 FLAIR image may show gliosis.

51. mucopolysaccharidosis

53. Cystic Neoplasms
 Giant dilatations of the VR spaces may cause
mass effect and assume bizarre configurations
that may be misinterpreted as a cystic brain
tumor.
 DD from VR spaces:
 Cystic brain tumors often have solid
components, may enhance with contrast
material, mostly show surrounding edema
 Contents are not equal to CSF (FLAIR images).

54. Cystic Neoplasms

56. Neurocysticercosis
 Cysticercosis is the most common parasitic
infection of the central nervous system
 Fluid-filled oval cysts with an internal scolex
(cysticerci) may be located in the brain
parenchyma.
 MR imaging findings of neurocysticercosis
are variable, depending on the stage of
evolution of the infection.

57. Neurocysticercosis
 In the granular nodular stage, a thickened retracted
cyst wall is seen, which may have nodular or ring
enhancement. Edema decreases.

58. Neurocysticercosis
 In the initial vesicular stage, a cystic lesion is
isointense to CSF with all MR sequences, resembling
an enlarged VR space. However, a discrete eccentric
scolex (hyperintense to CSF) may be seen.

59. Neurocysticercosis
 In the colloidal vesicular stage, the cyst is mildly
hyperintense to CSF. Mild to marked surrounding
edema may be seen. A thick cyst wall enhances,
including the scolex

60. Neurocysticercosis

62. Arachnoid cysts
 Arachnoid cysts represent intra-arachnoid CSF–
containing cysts that do not communicate with the
ventricular system.
 The most common locations are the middle cranial
fossa, the perisellar cisterns, and the subarachnoid
space over the convexities.
 DD from VR spaces:
Their typical location.

63. Arachnoid cysts

65. Neuroepithelial Cysts
 Neuroepithelial cysts are rare and benign
lesions.
 They have the same CSF signal intensity
DD from VR spaces:
Certainty only by pathologic study.

66. Neuroepithelial Cysts

67. Normal Aging

68. Normal Aging
In normal aging we can see:
1- Periventricular caps and bands
- Periventricular caps are hyperintense
regions around the anterior and posterior pole
of the lateral ventricles and are associated with
myelin pallor and dilated perivascular spaces.

69. -Periventricular
bands or 'rims'
are thin linear
lesions along the
body of the
lateral ventricles
and are
associated with
subependymal
gliosis.

70. 2-Mild atrophy with widening of sulci
and ventricles
3-Punctate and sometimes even
confluent lesions in the deep white
matter (Fazekas I and II).

71. Fazekas classification
The Fazekas classification is used to describe
changes in the deep white matter.
Fazekas I : small punctate lesions in the deep
white matter
Fazekas II : larger WMLs that are beginning to
become confluent.
Fazekas III : extensive confluent WMLs.

73. Fazekas I
is considered normal in aging.
Fazekas II
is considered abnormal in patients < 75 Years.
Fazekas III
is abnormal in any age group.
These WMLs are probably due to
microangiopathy and seen more frequently in
patients with vascular risk factors .

74. Thank you