FOR RADIOLOGY USEFULL FOR NEW RADIOLOGY RESIDENTS TO INDENTIFY NORMAL ANATOMY AND ABNORMAL FINDINGS IN BRAIN CT AND MRI SCANS. IN EMERGANCY CASES AND IN ROUTINE OPD IPD PATIENDS

1.  DR VAIBHAVI PATEL
 DNB RESIDENT
 APOLLO HOSPITAL
 GANDHINAGAR
This Photo by Unknown author is licensed under CC BY.

2. MODALITES OF BRAIN SCAN
• COMPUTED TOMOGRAPHY.
• MAGNETIC RESONANCE IMAGING
• NON CONTRAST CT AND MRI
• CONTRAST ENHANCED CT AND MRI
• ON CT SCAN ,
• BRAIN SOFT TISSUE WINDOW – W:80 L:40
• BONE WINDOW – W:1800-L:400

3. PLANES OF IMAGING

41. • Sulcal effacement
• Sulcal effacement is the term used to describe the loss of
the normal gyral-sulcal pattern of the brain, which is
typically associated with raised intracranial pressure.
• Grey-white matter differentiation
• On a normal CT head scan, the grey and white matter
should be clearly differentiated. Loss of this
differentiation suggests the presence of oedema which
may develop secondary to a hypoxic brain injury,
infarction (e.g. ischaemic stroke), tumour or cerebral
abscess.

49. Watershed Infarcts :
-Watershed infarcts occur at the border
zones between major cerebral arterial territories as
a result of hypoperfusion​
-There are two patterns of border zone infarcts:​
1-Cortical border zone infarctions :
-Infarctions of the cortex and
adjacent subcortical white matter located at the border
zone of ACA / MCA and MCA / PCA

50. 2-Internal border zone infarctions :
-Infarctions of the deep white matter of the centrum
semiovale and corona radiata at the border
zone between lenticulostriate perforators and the deep
penetrating cortical branches of the MCA
or at the border zone of deep white matter branches
of the MCA and the ACA

52. A patient with an occlusion of the right internal carotid artery ,
the hypoperfusion in the right hemisphere resulted in
multiple internal border zone infarctions, this pattern of
deep watershed infarction is quite common and should urge
you to examine the carotids

53. Small infarctions in the right hemisphere in the deep border zone (blue arrowheads)
and also in the cortical border zone between the MCA & PCA territory (yellow
arrows) , there is abnormal signal in the right carotid (red arrow) as a result of
occlusion

54. Lacunar Infarcts :
• Lacunar infarcts are small infarcts (15 mm or
less)in the deeper parts of the brain (basal
ganglia , thalamus , white matter) and in the
brain stem
• -Lacunar infarcts are caused by occlusion of
a single deep penetrating artery
• - M.C Cause Atherosclerosis

56. T2W- and FLAIR image of a Lacunar infarct in the left thalamus , on the
FLAIR image the infarct is hardly seen , there is only a small area of
subtle hyperintensity
Major differential is VR Spaces (Virchow Robin spaces) -Interstial
fluid spaces
More regular and has CSF SIGNAL INTENSITY ON ALL MRI SEQUENCES
,Suppresses on FLAIR

58. Grading of leukoaraiosis severity based on the Fazekas
scale.
(A) Fazekas grade 1 (mild) with periventricular caps of the
ventricles or punctate foci in the deep white matter
(B) Fazekas grade 2 (moderate) with smooth
periventricular halo or convergence of deep white matter
lesions
(C) Fazekas grade 3 (severe) with confluent periventricular
leukoaraiosis extending into the subcortical deep white
matter.

60. Acute Arterial Infarct – MRI
Appearance
-Diffusion Abnormality
-Absent Arterial FlowVoid -Increased T2 Signal due
to edema and Mass Effect
Intravascular Stasis of ContrastMedium -
Reduced Perfusion
-Arterial Occlusion
-Meningeal Enhancement -Hemorrhage
-Wallerian Degeneration

61. 1-Normal CT:
-Initial appearances often normal in first few hours , larger
infarcts more prominent
-Initial Signs :
1.Low Density Region​
2.Mass Effect​
3.Hyperdense Artery
a) Low Density Region :
1-Loss of grey / white matter differentiation is a feature of
acute infarction and is the earliest radiological
abnormality (thought to be due to decreased cerebral
blood volume)

62. Normal GWM differentiation Loss of GWM differentiation

63. 3-The (insular ribbon sign) is a finding of early
MCA infarction describes the loss of gray-
white matter differentiation in the insula ,
the normal striated appearance of this area is
replaced by a swollen homogeneous area of
low attenuation

64. Insular ribbon sign , -
this refers to
hypodensity and
swelling of the insular
cortex , it is a very
indicative and subtle
early CT-sign of
infarction in the
territory of the MCA
This region is very-
sensitive to
ischaemia following
MCA occlusion than
other portions of the
MCA territory
because it has the
least potential for
collateral supply from
the ACA & PCA

66. Cytotoxic edema leads to hypoattenuation such that the
normal insular ribbon is no longer visible (blue arrows)
EARLY LATE

67. Alternatively , the basal
ganglia may disappear
as the infarcted grey
matter acquires the
same CT attenuation
as the surrounding
white matter ,
obscuration of the
lentiform nucleus
(putamen & globus
pallidus) is caused by
loss of gray-white
matter differentiation
at the border of the
lentiform nucleus and
the posterior limb of
the internal capsule

68. Diffusion Abnormality on MRI:
-Abnormalities may be seen within minutes of
arterial occlusion with diffusion-weighted MRI
-Standard diffusion protocol includes a DWI and an
apparent diffusion coefficient (ADC) image ,
these are usually interpreted side by side

69. Sequence Hyperacute(<6
hr)
Acute (>6 hr) Subacute
(Days to
Weeks)
Chronic
DWI High High High (decrease
with time)
Isointense to
bright
ADC Low Low Low to Isointense to
isointense bright
T2 / FLAIR Isointense Slightly bright Bright Bright
to bright
T1 Subtle Hypointense Hypointense Hypointense
hypointensity

70. -In the acute phase T2WI will
be normal but in time the
infarcted area will become
hyperintense. The
hyperintensity on T2WI
reaches its maximum
between 7 and 30 days after
this it starts to fade
DWI is already positive in the
acute phase and then
becomes more bright with a
maximum at 7 days , DWI in
brain infarction will be
positive for approximately for
3 weeks after onset (in spinal
cord infarction DWI is only
positive for one week)
-ADC will be of low signal
intensity with a maximum at
24 hours and then will
increase in signal intensity
and finally becomes bright
in the chronic stage

71. a) Hyperacute Infarct (0-6 hours) :
-Within minutes of critical ischemia , the sodium-
potassium ATPase pump that maintains the normal
low intracellular sodium concentration fails , sodium
& water diffuse into cells leading to cell swelling
and cytotoxic edema causing restricted diffusion.
-Calcium also diffuses into cells which triggers cascades
that contribute to cell lysis
-Diffusion is the most sensitive modality , DWI
hyperintensity & ADC map hypointensity reflect
reduced diffusivity which can be seen within minutes
of the ictus

72. Hyperacute Infarct
T1
T1 T2 DWI ADC
Hyperacute Infarct

73. b) Acute Infarct (6-72 hours) :
-The acute infarct is characterized by increase in
vasogenic edema and mass effect
-Damaged vascular endothelial cells cause leakage of
extracellular fluid and increase the risk of
hemorrhage
-On imaging , there is increased sulcal effacement and
mass effect , the mass effect peaks at 3-4 days
which is an overlap between the acute & early
subacute phases

74. -MRI shows hyperintensity of the infarct core on T2 ,
best seen on FLAIR , the FLAIR abnormality is usually
confined to the grey matter , DWI continues to show
restricted diffusion
-There may be some arterial enhancement due
to increased collateral flow
-

75. Acute Left MCA Infarct
T1 DWI ADC

76. c) Early Subacute Infarct (1.5 days-5 days) :
-In the early subacute phase , blood flow to the
affected brain is re-established by leptomeningeal
collaterals and ingrowth of new vessels into the
region of infarction
-The new vessels have an incomplete blood brain
barrier causing a continued increase in
vasogenic edema & mass effect which peaks at
3-4 days
-MRI shows marked hyperintensity on T2 involving both
grey & white matter (in contrast to the acute phase
which usually involves just the grey matter)

77. d) Late Subacute Infarct (5 days-2 weeks) :
-The subacute phase is characterized by resolution of
vasogenic edema and reduction in mass effect
-A key imaging finding is gyriform enhancement which
may occasionally be confused for a neoplasm ,
unlike a tumor , subacute infarction will not typically
show both mass effect and enhancement
simultaneously , enhancement be seen from
approximately 6 days to 6 weeks after the initial
infarct
-Diffusion may remain bright due to T2 shine through
, although ADC map will either return to normal or
show increased diffusivity

78. Enhancing infarcts , T1+C shows gyriform enhancement at the left insula and
posterior parietal lobe from a late subacute left MCA infarct

79. b) Mass Effect :
-Local effacement of the cerebral sulci and
fissures may be followed by more diffuse
brain swelling
-Maximal swelling usually occurs after 3-5 days
-Infarcts that do not have a typical appearance
must be differentiated from other solitary
intracranial masses

82. -Increased T2 Signal :Edema and mass efffect
-T2W signal change represents cytotoxic
edema and typically becomes visible by 3-6
hours
-The earliest changes are identified within the
grey matter structures , accompanied by a
reduction in T1W signal

84. Hyperdense artery :
-Represents acute thrombus within the vessel
-Most commonly recognized with basilar
and proximal MCA thrombosis
-False positives can occur if a vessel is partially
calcified or if the haematocrit is raised (i.e.
polycythaemia)

85. On the left a patient with a dense MCA sign-
-On CTA : occlusion of the MCA is visible

87. Gradient Echo shows blooming artifact (red arrow) in the right proximal MCA
which represents intraluminal thrombus and in the MRI correlate to the
hyperdense artery sign that can be seen on CT

88. -Absent Arterial Flow Void :
-An immediate sign of vessel occlusion best
seen on T2W and FLAIR imaging
-An occluded vessel returns high signal on these
sequences

89. Left MCA thrombus , the left MCA shows high signal from an intraluminal clot
on FLAIR (a) but low signal on gradient recalled echo (GRE) T2* (b) , this
corresponds to a filling defect (arrow) on CT angiogram (c) , a subtle FLAIR
high signal is present at the left insula

90. Arterial Occlusion :
-CT angiography may demonstrate stenosis or
complete arterial occlusion prior to
spontaneous recanalization

91. Demonstrates absence-
of contrast enhancement
at the left MCA
distribution and
decreased left cerebral
hemispheric arterial
collateralization
compared to the right
cerebral hemisphere
The intensity of the-
vessels on the left is
decreased as compared
with those on the right

93. Hemorrhage :
-Frank hemorrhage into an arterial infarct
typically occurs a few days after the initial
stroke.
-If there is hemorrhage within an infarct from
the outset , a venous stroke or arterial
embolus should be considered

95. -Hemorrhagic transformation with foci of hemorrhage
at the right post central gyrus

97. CT , Hemorrhagic evolution of initial ischemic infarction with
significant midline shift

98. Petechial hemorrhages on MRI :
-Usually appear as the name suggests , as tiny
punctate regions of hemorrhage often not able
to be individually resolved but rather resulting in
increased attenuation of the region on CT of
signal loss on MRI , although this petechial
change can result in cortex appearing near
normal it should not be confused with the
phenomenon of fogging seen on CT which occurs
2 to 3 weeks after infarction

99. -Petechial hemorrhage typically is more
pronounced in grey matter and results in
increased attenuation
-This sometimes mimics normal grey matter
density and contributes to the
phenomenon of fogging

100. Petechial hemorrhage , gyriform low signal in the right frontal
lobe (arrow) on this GRE T2* corresponds to susceptibility
from petechial hemorrhage in an acute infarct

101. N.B. :
Fogging Phenomenon
-Is seen on non contrast CT of the brain and
represents a transient phase of the evolution of
cerebral infarct where the region of cortical
infarction regains a near normal appearance
-During the first week following a cortical infarct
hypoattenuation and swelling become
more marked resulting in significant mass effect
and clear demarcation of the infarct with vivid
gyral enhancement usually seen at this time

102. -As time goes on the swelling starts to subside and
the cortex begins to increase in attenuation , this is
believed to occur as the result of migration into
the infarcted tissue of lipid-laden macrophages as
well as proliferation of capillaries and decrease in
the amount of edema
-After 2 to 3 weeks following an infarct the cortex
regains near-normal density and imaging at this
time can lead to confusion or missed diagnosis

103. -Fogging has been demonstrated in around 50% of
cases
-If in doubt the administration of IV contrast
will demarcate the region of infarction
-A similar phenomenon is also seen on T2 weighted
sequences on MRI of the brain and is believed to
be due to similar cellular processes, as the timing
is similar , it has been found to occur in
approximately 50% of patients between 6 and 36
days (median 10 days) after onset of infarction

104. 2 Days post onset of
symptoms
9 days post onset of symptoms

105. Contrast Enhancement :
-Usually occurs by 4 days and reflects
impairment of the blood-brain barrier
-Typically gyriform (following the cerebral cortex)
but may appear ring-enhancing or confluent
-Subsides by 4-8 weeks
-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

106. -Enhanced CT images of a
patient with an infarction
in the territory of the MCA
-There is extensive
gyral enhancement
(luxury perfusion)
-Sometimes this luxury
perfusion may lead to
confusion with tumoral
enhancement
-Luxury perfusion used to
describe the dilation of
numerous vascular
channels observed within
the relatively avascular
infarcted area of the
brain 24-48 h after an
ischemic stroke , these
are predominantly
venous channels but
arterial channels open up
as well

107. Intravascular Stasis of Contrast Medium :
-Prolonged transit of contrast medium
through distal / collateral vessels causes
high arterial signal on post-gadolinium T1W
images

108. Arterial enhancement from infarct , T1+C shows increased
enhancement of the left MCA vessels in this hyperacute
infarct

109. 4 hrs after left MCA symptoms began , extensive Intravascular
enhancement seen (an immediate finding)

110. Chronic Infarct :
-In the chronic stage of infarction , cellular debris and
dead brain tissue are removed by macrophages
and replaced by cystic encephalomalacia and
gliosis
-Infarct involvement of the corticospinal tract may
cause mass effect , mild hyperintensity on T2 and
eventual atrophy of the ipsilateral cerebral peduncle
& ventral pons due to Wallerian degeneration ,
these changes can first be seen in the subacute
phase with atrophy being predominant feature in
the chronic stage (See later)

111. -DWI has usually returned to normal in the
chronic stages
-Occasionally , cortical laminar necrosis can
develop instead of encephalomalacia , cortical
laminar necrosis is a histologic finding
characterized by deposition of lipid-laden
macrophages after ischemia that manifests
on imaging as hyperintensity on both T1 & T2

112. DWI shows an area of low signal intensity in the right occipital lobe (arrow)
with a peripheral rim of high signal intensity , a finding that may be due to
T2 shine-through

113. ADC map shows a corresponding area of high signal intensity
(arrow)

114. T1 shows a corresponding area of low signal intensity (arrow)

115. T2 shows an area of high signal intensity in the right occipital
lobe (arrow)

116. T1+C shows a corresponding area of parenchymal enhancement
(arrow)

117. -Wallerian Degeneration :
a) Incidence
b) Radiographic Features

118. a) Incidence :
-Appears in the chronic phase of
cerebral infarction (> 30 days)
-Frequently observed in the corticospinal
tract following infarction of the motor
cortex or internal capsule

119. c) Radiographic Features :
-Hyperintensity on T2-weighted images along the affected
tracts
-Conventional MRI depict WD when sufficiently large bundles of
fibers are involved along the corticospinal tract , the corpus
callosum , fibers of the optic radiations , fornices and
cerebellar peduncles
---Shows diffusion restriction

120. Coronal T2 shows hyperintensity of left corticospinal tract due to
wallerian degeneration

121. Axial T2 shows Bilateral and symmetric hyperintensities of
pontocerebellar tract (arrows)

129. Abnormal shifts of brain
tissue
• Look for abnormal shifts of brain tissue and/or
herniation:
• Subfalcine: beneath the falx cerebri
• Uncal: inferomedial displacement of the uncus
• Transcalvarial: brain shift through the calvarium
• Transtentorial: may be superior or inferior
• Tonsillar: downward displacement of the
cerebellar tonsils into the foramen magnum

130. Hypo/hyperdense foci
• Hypodense foci
• Hypodensity on a CT head may be due to the
presence of air, oedema or fat:
• Oedema is often seen surrounding
intracerebral bleeds, tumours and abscesses.
• Pneumocephalus (air within the cranial vault)
may be noted after neurosurgery or adjacent
to the inner table in cases of calvarial
fractures.

133. Other common findings
on routine brain scans
• Cerebral Cortical Atrophy
• Small vessel ischemic changes
• Encephalomalacia
• Arachnoid cysts
• Mega cisterna magna
• Subdural hygroma
• Porencephalic cyst
• Variants of septum pallucidum.
• Hydrocephalus

134. Cerebral atrophy
• Brain parenchymal volume loss
• a common finding in the elderly population,
• involutional" or "age-related" when the patient
has normal cognition.
• the compensatory enlargement of the CSF
spaces from reducing brain parenchymal volume,
• hydrocephalus ex vacuo- focal volume loss in
the brain following a pathological insult (i.e.
hemorrhage) rather than the often idiopathic
more generalized changes seen with age.

135. Radiographic features
• Characteristic features include prominent cerebral
sulci (i.e. cortical
atrophy) and ventriculomegaly (i.e. central atrophy)
without bulging of the third ventricular recesses.
• It can be difficult to distinguish this from the
changes seen in normal pressure hydrocephalus.

136. • Certain important patterns of cerebral atrophy that
are more specific include:
• severe frontal and anterior temporal
• Pick disease
• head of caudate nuclei
• Huntington disease
• posterior parietal and frontal
• corticobasal degeneration

137. • atrophy of tectum, globus pallidus, and
frontal lobes
• progressive supranuclear palsy
• generalized with atrophy of substantia nigra
• Parkinson disease
• severe hippocampal atrophy
• Alzheimer dementia

138. CT images demonstrate marked prominence of
the ventricles and sulci. This is consistent with
cerebral atrophy.

139. Hydrocephalus
• Hydrocephalus merely denotes an increase in the volume
of CSF and thus of the cerebral ventricles (ventriculomegaly).
• Types
• Types of hydrocephalus are as follows
• communicating (i.e. CSF can exit the ventricular system)
• non-communicating (i.e. CSF cannot exit the ventricular system,
and thus there is by definition obstruction to CSF absorption)-
obstructive hydrocephalus

141. Radiographic features
• CT
• Bicaudate index is larger than 95th percentile on age 5
•The bicaudate index is the ratio of width of two lateral
ventricles at the level of the head of the caudate nucleus to
distance between outer tables of skull at the same level. It can
be a useful marker of ventricular volume and in the diagnosis
of hydrocephalus.
• Axial width of temporal horn lateral ventricle more
than or equal to 5 mm 5

142. Normal pressure
hydrocephalus
• characterized by the triad of gait
apraxia/ataxia, urinary incontinence, and
dementia.
• On imaging, it can be characterized both on CT
and MRI by enlarged lateral and third
ventricles out of proportion to the cortical
sulcal enlargement.

143. Morphological changes
ventriculomegaly
• increased Evans' index >0.3
• ratio of the maximum width of the frontal horns of
the lateral ventricles and the maximal internal
diameter of the skull at the same level employed in
axial CT and MRI images.
• widening of the temporal horns of the lateral
ventricles >6 mm
• acute callosal angle
• upward bowing of the corpus callosum

144. • disproportionate changes in subarachnoid spaces
• dilated Sylvian fissures
• tight high convexity (narrow sulci and
subarachnoid spaces at the vertex and
medial/parafalcine region)
• cingulate sulcus sign: posterior half of cingulate sulcus
is narrower than the anterior half
• focal/isolated dilation of sulci over the medial surface
or convexity (sometimes called transport sulci)

145. Several signs of normal
pressure hydrocephalus:
• narrow callosal angle of 74
degrees
• coronal T2: periventricular
edema (green arrows)
• sagittal T1: wide cerebral
aqueduct (red arrow) and
normal floor of the 3rd
ventricle (green arrow)
• axial T2: increased flow void
in the aqueduct (green
arrow)
• axial T2: narrow parasagittal
CSF fissures (green arrows)
• axial T2: wide Sylvian fissures
(green arrows)

146. Hydrocephalus versus atrophy
• Features that favor hydrocephalus include:
• dilatation of the temporal horns
• lack of dilatation of parahippocampal fissures 4
• increased frontal horn radius
• acute ventricular angles
• periventricular interstitial edema from
the transependymal flow

147. • intraventricular flow void from CSF movement on
MRI
• widening of the third ventricular recesses:
midsagittal plane
• upward displacement of corpus callosum 3:
midsagittal plane
• depression of the posterior fornix: midsagittal
plane
• decreased mamillopontine distance: midsagittal
plane
• narrow callosal angle
• cingulate sulcus sign

148. Encephalomalacia
• any area of cerebral parenchymal loss with or
without surrounding gliosis.
Clinical presentation
•asymptomatic
•serve as a focus of seizure

149. Radiographic features
CT
• hypoattenuation, somewhat, higher than CSF
• volume loss
• often associated with gliosis and Wallerian degeneration
• MRI
• Follows CSF signal on all sequences including FLAIR.
• T1: low signal
• T2: high signal, attenuating fully on FLAIR
• ADC: facilitated diffusion

150. Evidence of old left MCA territory
infarct with encephalomalacia and
surrounding gliosis. There is ex vacuo
dilatation of the left lateral ventricle.

151. Porencephaly
• Porencephaly is a rare congenital disorder that
results in cystic degeneration
and encephalomalacia and the formation
of porencephalic cysts.
• a cleft or cystic cavity within the brain
• a focal cystic area of encephalomalacia that
communicates with the ventricular
system and/or the subarachnoid space.

152. Focal atrophy in the right parietal lobe with replacement by a cystic mass that
communicates with the right lateral ventricle causing mass effect on the
overlying skull vault leading it to be bowed out. It could be an arachnoid cyst but
communicates with the ventricle thus the mass effect on the inner table of the
vault by CSF pulsation. It is not open lip schizencephaly as the defect is not grey
matter lined.

153. Arachnoid cyst
• Common benign and asymptomatic lesions
• Located within the subarachnoid space and
contain CSF.

154. On imaging
• Well circumscribed cysts with an
imperceptible wall, displacing adjacent
structures, and following CSF density on CT
and CSF signal intensity on MRI (i.e.
hyperintense on T2-weighted images with
FLAIR suppression).
• Remodeling effect on adjacent bone.

155. Fluid density extra axial cyst like lesion is seen
at right frontal region which causes remodeling
of the adjacent bone.

156. MRI through the posterior fossa demonstrates a large
right-sided extra-axial CSF intensity mass lesion. It
follows CSF on all sequences, including FLAIR and
DWI/ADC. There is significant mass effect on the
adjacent cerebellar tissue and remodelling and
expansion of the adjacent skull is evident.

157. Mega cisterna magna
• a normal variant characterized by a truly focal
enlargement of the CSF-filled subarachnoid
space in the inferior and posterior portions of
the posterior cranial fossa.

158. CT/MRI
 prominent retrocerebellar cerebrospinal fluid
(CSF) appearing space with a normal vermis,
normal 4th ventricle, and normal cerebellar
hemispheres.
 An enlarged cisterna magna usually measures
>10 mm on midsagittal images.

159. Prominent retrocerebellar
CSF space.
Large retrocerebellar space
that follows CSF signal on all
sequences. Normal cerebellar
vermis.
AXIAL T2

160. ARACHNOID CYST
• Slow
comminucation with
ventricles/subarachnoid
space.
• Hydrcephalus and mass
effect
MEGA CISTERNA
MAGNA
• Freely communicates . On
cisternography.
• Mostly asmyptomatic

161. Subdural hygroma
• the accumulation of fluid in the subdural
space.
• idiopathic: in pediatric patients
• trauma: may occur either as an acute or
chronic phenomenon 10-11
• post surgical, e.g. hematoma evacuation,
ventricular drainage
• spontaneous intracranial hypotension

162. CT/MRI
• A crescentic near-CSF density/signal accumulation in the
subdural space that does not extend into the sulci.
• rarely exerts significant mass-effect.
• Do not entirely follow CSF on FLAIR, often appearing
hyperintense.
• Vessels rarely cross through the lesion in contrast-enhanced
studies .
• Cortical vein sign: the presence of superficial cortical veins
seen on MRI and CT (particularly with contrast
injection) traversing an enlarged subarachnoid space,

163. Differential diagnosis
• chronic subdural hematoma
• cerebral atrophy
• arachnoid cyst
• benign enlargement of the subarachnoid
spaces in infancy

164. Cavum septum pellucidum
• Cavum septum
pellucidum (CSP) is
a normal
variant CSF space
between the
leaflets of
the septum
pellucidum.

165. Cavum vergae
• the posterior extension of the cavum septum
pellucidum.
• posterior to the anterior columns of
the fornix, lying anterior to the splenium of
the corpus callosum.
• it may exist independently.

166. A cavum septum pellucidum and
associated cavum vergae.

167. Cavum veli interpositi
• a dilatation of the normal cistern of the velum
interpositum -
• Velum intepositum : - a small membrane
containing a potential space just above and
anterior to the pineal gland which can become
enlarged to form a cavum velum interpositum.

168. CT/MRI
• an enlarged CSF space situated between
the atria/trigones of the lateral ventricles,
behind the foramen of Monro, beneath the
columns of the fornices and above the tela
choroidea of the 3rd ventricle.

169. On axial imaging, it is
triangular in shape.

170. Thank you