CT BRAIN / MR – An introduction to
Normal Anatomy, Interpretation and
Some Common Pathologies
Associate Professor & Consultant Radiologist
Dept of Radiology and Imaging Sciences
Sri Ramachandra Medical College & Research Institute
in 1/3 MCA
Purpose of imaging in stroke
Definite diagnosis of stroke.
To document the presence or absence of
This information is critical since
anticoagulation is a standard therapy for
Identify ischemic penumbra
Assess location & extent of brain damage
(e.g. impending herniation)
To exclude stroke mimics.
CT in Hyperacute Stroke ( 0-6 hrs )
Not v.sensitive for infarction
Sensitive for a/c hemorrhage & gross
lesions precluding thrombolytic therapy
20 % within 2 hrs
82 % within 6 hrs
Hyperacute Stroke On CT
EARLY ISCHEMIC CHANGES
Hyperdense vessel sign
Attenuation of lentiform
Loss of insular ribbon
Effacement of sulci
Significance of Early Ischemic Signs
No contraindication to thrombolysis
Patel et al JAMA 2001;286:2830–2838
Indicate more extensive ischemia
Hyperdense vessel sign
Obscuration of basal ganglia
Loss of grey-white matter interface
Effacement of sulci
Strong association with later hemorrhagic
transformation AJNR 1991;12:1115-1121
Subacute infarct (1-7 days )
Hemorrhagic transformation in 5-40 % of all
ischemic stroke Neurology 2001; 57:1603-1610
Hypertensive hemorrhage accounts for
approximately 70-90% of non-traumatic primary
intracerebral hemorrhages. It is commonly due to
vasculopathy involving deep penetrating arteries
of the brain. Hypertensive hemorrhage has a
predilection for deep structures including the
thalamus, pons, cerebellum, and basal ganglia,
particularly the putamen and external capsule.
Thus, it often appears as a high-density
hemorrhage in the region of the basal ganglia.
Blood may extend into the ventricular system.
Intraventricular extension of the hematoma is
associated with a poor prognosis.
Hemorrhages can occur in the intraparenchymal,
subarachnoid, intraventricular, subdural and
Location of hypertensive hemorrhage:
Putamen, external capsule, thalamus, pons,
cerebellum, subcortical white matter
In the absence of trauma, the most common cause
of subarachnoid hemorrhage is a ruptured cerebral
aneurysm. Cerebral aneurysms tend to occur at
branch points of intracranial vessels and thus are
frequently located around the Circle of Willis.
Common aneurysm locations include the anterior
and posterior communicating arteries, the middle
cerebral artery bifurcation and the tip of the basilar
artery. Subarachnoid hemorrhage typically presents
as the "worst headache of life" for the patient.
Detection of a subarachnoid hemorrhage is crucial
because the rehemorrhage rate of ruptured
aneurysms is high and rehemorrhage is often fatal.
CT is currently the imaging modality of choice because
of its high sensitivity for the detection of subarachnoid
hemorrhage. CT is most sensitive for acute
subarachnoid hemorrhage. After a period of days to
weeks CT becomes much less sensitive as blood is
resorbed from the CSF. If there is a strong clinical
indication, LP may be warranted despite a negative CT
since small bleeds can be unapparent on imaging.
On CT, a subarachnoid hemorrhage appears as high
density within sulci and cisterns. The insular regions
and basilar cisterns should be carefully scrutinized for
subtle signs of subarachnoid hemorrhage.
Subarachnoid hemorrhage may have associated
intraventricular hemorrhage and hydrocephalus.
Venous Sinus Thrombosis with Venous
Clinical symptoms – head ache, seizures
Pathology is due to decrease in perfusion pressure as
the venous pressures elevate due to occlusion.
Predisposing conditions are dehydration, infection,
polycythemia, sickle cell disease, hypercoagulable
states, peripartum, OCP poisoning.
Unilateral / bilateral parenchymal hypodensities
Not limited to an arterial territory
May be associated with hemorrhage
Signs: Delta sign, Enhancement of walls of sinus than
Dynamic study depicting intracellular
metabolism of cerebral ischemia.
Within the region of infarct, lactate
appears elevated whereas NAA and
total creatinine are reduced.
Radionucleotide studies in acute
PET is an accurate method of quantifying
changes in cerebral hemodynamics.
As cerebral blood flow (CBF) falls, cerebral
blood volume (CBV) and oxygen extraction
factor (OEF) increase.
PET measures changes in CBF, CBV and OEF
Plays a limited role due to limited availability .
SPECT with Tc 99m HMPAO or ECD will show
a perfusion defect.
Radionucleotide Studies in Acute Stroke
SPECT – Tc99m HMPAO
PET – O15
Adv – Early detection
Limitation - Not widely
MRI has been increasingly utilized in
early stroke since it is more sensitive
than CT in the first twelve hours
Bright on Diffusion weighted images
(detected as early as 15 to 30 min after
CT / MR Perfusion imaging
Concentrates on the assessment of mean
transit time (MTT), relative cerebral blood
volume (RCBV) and derived relative cerebral
blood flow. RCBF = MTT / RCBV
Prolonged MTT is the earliest & most consistent
sign of impaired perfusion.
In addition to this, there is a simultaneous drop
in RCBV indicating tissue at risk for infarction.
Stroke in Children Constitutes 3% of cerebral infarcts
Most common cause is congenital heart
disease. Other causes are vasospasm &
Echo, CT, MRI & catheter angiogram
should be performed as and when
There are several advantages to performing a CT scan
instead of other imaging modalities. A CT scan:
- Is readily available
- Is rapid
- Allows easy exclusion of hemorrhage
- Allows the assessment of parenchymal damage
The disadvantages of CT include the following:
- Old versus new infarcts is not always clear
- No functional information (yet)
- Relatively limited evaluation of vertebrobasilar system
A CT is 58% sensitive for infarction within the first 24 hours
(Bryan et al, 1991). MRI is 82% sensitive. If the patient is
imaged greater than 24 hours after the event, both CT and
MR are greater than 90% sensitive.
An epidural hematoma is usually associated with a skull
fracture. It often occurs when an impact fractures the
calvarium. The fractured bone lacerates a dural artery or a
venous sinus. The blood from the ruptured vessel collects
between the skull and dura. On CT, the hematoma forms a
hyperdense biconvex mass. It is usually uniformly high
density but may contain hypodense foci due to active
bleeding. Since an epidural hematoma is extradural it can
cross the dural reflections unlike a subdural hematoma.
However an epidural hematoma usually does not cross
suture lines where the dura tightly adheres to the adjacent
Cerebral contusions are the most common
primary intra-axial injury. They often occur
when the brain impacts an osseous ridge or a
dural fold. The foci of punctate hemorrhage
or edema are located along gyral crests. The
following are common locations:
- Temporal lobe - anterior tip, inferior
surface, sylvian region
- Frontal lobe - anterior pole, inferior surface
- Dorsolateral midbrain
- Inferior cerebellum
Cerebral Contusion On CT, cerebral contusion
appears as an ill-defined
hypodense area mixed with
foci of hemorrhage.
hemorrhage is common.
After 24-48 hours,
coalescence of petechial
hemorrhages into a
rounded hematoma is
Diffuse Axonal Injury
Diffuse axonal injury is often referred to as "shear injury". It is the most
common cause of significant morbidity in CNS trauma. Fifty percent of all
primary intra-axial injuries are diffuse axonal injuries. Acceleration,
deceleration and rotational forces cause portions of the brain with
different densities to move relative to each other resulting in the
deformation and tearing of axons. Immediate loss of consciousness is
typical of these injuries. The CT of a patient with diffuse axonal injury may
be normal despite the patient's presentation with a profound neurological
deficit. With CT, diffuse axonal injury may appear as ill-defined areas of
high density or hemorrhage in characteristic locations. The injury occurs in
a sequential pattern of locations based on the severity of the trauma. The
following list of diffuse axonal injury locations is ordered with the most
likely location listed first followed by successively less likely locations:
- Subcortical white matter
- Posterior limb internal capsule
- Corpus callosum
- Dorsolateral midbrain
Encephalitis CT scan is often normal , especially early in
Ill defined hypodense lesions may be seen
e.g. temporal lobe changes are predominant
in Herpes Encephalitis.
MRI is far more sensitive in the evaluation of
patients with encephalitis
Skull fractures are categorized as linear or depressed,
depending on whether the fracture fragments are
depressed below the surface of the skull. Linear
fractures are more common. The bone windows must
be examined carefully. A skull fracture is most clinically
significant if the paranasal sinus or skull base is
involved. Fractures must be distinguished from sutures
that occur in anatomical locations (sagittal, coronal,
lambdoidal) and venous channels. Sutures have
undulating margins both sutures and venous channels
have sclerotic margins. Venous channels have
undulating sides. Depressed fractures are characterized
by inward displacement of fracture fragments.
Ventriculitis / Ependymitis
Inflammation and enlargement of the
ventricles characterizes ventriculitis.
Ependymitis shows hydrocephalus with
damage to the ependymal lining and
proliferation of subependymal glia. A CT of
patients with these conditions reveals the
presence of periventricular edema and
subependymal enhancement. Ventriculitis and
Ependymitis affect approximately 30% of the
adult patients and 90% of the pediatric
patients with meningitis.
Cerebrovascular Complications of
The development of cerebrovascular problems is
the most common complication of meningitis.
Arterial infarction can occur which often affects
the basal ganglia due to the occlusion of small
perforating vessels. Hemispheric infarction can
also occur due to major vessel spasm. Venous
infarctions are also common and can include
cortical venous occlusion or the involvement of
the superior sagittal sinus.
Subdural empyema is usually due to
meningitis, sinusitis, trauma or prior surgery.
It is a neurosurgical emergency. Subdural
empyema leads to rapid clinical deterioration,
especially if it is due to sinusitis. On CT it
appears as an isodense or hypodense extra-
axial mass. It has a lentiform or crescentic
The margin of collection often enhances with
contrast material administration due to the
presence of granulation tissue or subjacent
Extra-axial CNS Infection
Extra-axial CNS infections can cause epidural
abscess or subdural empyema. Extra-axial CNS
infections account for 20-30% of CNS infections.
Fifty percent of extra-axial infections are
associated with sinusitis, usually frontal sinusitis.
The infection occurs by direct extension or septic
thrombophlebitis. Thirty percent of extra-axial
infections occur post-craniotomy. Finally, 10-15%
of extra-axial CNS infections are related to
meningitis. CT findings include a focal fluid
collection usually with an enhancing margin in a
subdural or epidural location.
Occurs due to obstruction of cerebral arteries or cerebral veins.
The clinical spectrum of ischemia includes
TIA (Transient ischemic attacks)
RIND (Reversible ischemic neurological deficit)
PRIND (partially reversible ischemic neurological
Normal cerebral blood flow to the brain cortex is approximately
50 to 66 ml/100gm/min. When cerebral perfusion pressure falls
below critical levels (<15ml/gm/min) ischemia results. Ischemia
produces energy depletion in the affected cells. This results in
accumulation of Ca++, Na+ and Cl-, along with osmotically
obligated water. This secondary accumulation of water results
in the imaging features of stroke such as edema and mass
Hyperdense vessel sign
Seen in 25% of stroke patients.
In patients presenting with clinical deficit
referable to the middle cerebral artery territory,
the hyperdense vessel sign is present 35-50% of
Lentiform Nucleus Obscuration
Due to cytotoxic edema in the basal
Indicates proximal middle cerebral
artery occlusion, which results in limited
flow to lenticulostriate arteries
Can be seen as early as one hour post
onset of stroke.
Insular Ribbon Sign
Loss of the gray-white interface at the lateral
margins of the insula.
Supplied by the insular segment of the middle
Particularly susceptible to ischemia because it
is the most distal region from either anterior
or posterior collaterals
May involve only the anterior or the posterior
Diffuse Hypodensity and Sulcal
Most consistent sign of infarction.
Extensive parenchymal hypodensity is associated
with poor outcome.
If > 50% of MCA territory involvement ,there is,
on average, an 85% mortality rate. Hypodensity
in greater than one-third of the middle cerebral
artery territory is generally considered to be a
contra-indication to thrombolytic therapy.
Cerebral Blood flow for Survival
Average blood flow : 55ml/ 100gm/ mt
Ischemic threshold : 20 ml/ 100gm/ mt
Tissue death : <10 ml/ 100gm/ mt
Functional failure without cell death:
10-20ml/ 100gm/ mt.
Concept of Ischemic Penumbra
Focal core area of infarct (irreversible)
Surrounded by viable neuronal cell on
the brink of cell death
Geographic area of tissue
surrounding a profoundly
ischemic core. Identified
on DWI / per MRI
Saving this potential
leads to significant
4 h 24 h
Dept. Neurosciences Univ. of Rome La Sapienza
Reversibility of Ischemic lesions on
Occlusion of MCA 1 hour - DWI lesion or resolution
Occlusion of MCA 2 hour - Lesion size same or
Successful thrombolysis may revert DWI changes
Diffusion changes in TIAs
• 29% to 67% will show restricted diffusion
• May reverse or persist
• Perfusion deficits
Stroke vs TIA
DWI lesions of TIA are less intense
Wiesmann M, et al. Eur Radiol.
MR Spectroscopy in acute stroke
Stroke 2003;34:e82-876 pts within 7 hrs of stroke onset
Lactate alone – metabolic injury - Reversible
Lactate + NAA- more severe – Irreversible
Lac/Cho ratio from acute lesions improves
the prediction of stroke outcome
25 yr old lady c/o fever and altered sensorium x 1
wk. Had 1 episode of GTC seizures. Admitted
elsewhere , LP done showed proteins-55 mg % and
sugar –105 mg % ..
ABG- pH – 7.55
HCO3 – 28.3 , PCO2-32.9, PO2 –322.9,SPO2-99.8
CT – Normal
Discharged at request.
H/o fever,headache and vomitting on and off x 5
CT Findings in Stroke
Hyperacute infarct (<12 hrs)
Normal (50 to 60%)
Obscuration of lentiform nucleus
Acute infarct (12 – 24hrs)
Loss of grey - white matter interface (insular
Low density basal ganglia
Hyperdense vessel sign
• Indicates poor outcome and poor response to iv - TPA therapy.
CT Findings in Stroke (Contd)…
Subacute infarct (1- 7days)
Wedge shaped hypodensity involving grey &
Chronic infarct ( 1 to 8 weeks)
Reduced mass effect
Global Cerebral Hypoperfusion
Consequence of global hypoperfusion.
Common causes are hypotension, cardiac
arrest with successful resuscitation, neonatal
asphyxia and CO inhalation.
1) Water shed infarct in the parieto-
occipital region & basal ganglia infarcts.
2) Cortical laminar necrosis with
hemorrhagic foci in basal ganglia & cerebral
3) In severe cases “reversal sign” is noted.
CT VS MRI in the setting of acute
MRI is more sensitive
Diffusion weighted MR images has the
highest sensitivity & specificity for acute
CT is more sensitive to detect
CT is more widely available in many
CT is less expensive
CT is more rapid
Useful in MCA embolic stroke & predictive of
infarction volume in MCA territory
Less useful –deep grey matter & brainstem
FLAIR + (GRE) T2*-weighted superior to
J Neurol Neurosurg
Combined MR Perfusion & Diffusion
In hyperacute stage, larger abnormality is
noted on the perfusion images than on
diffusion weighted images. This diffusion
perfusion mismatch is the ischemic
penumbra. This is the tissue at risk which
would benefit from thrombolysis.
To Summarize the Role of CT in
Haemorrhagic or non-haemorrhagic
Arterial or venous
Acute,subacute or chronic
Assess the mass effect
Exclude Stroke mimics like subdural
How the CT study is usually planned…
AIR - - 1000
FAT - - 30 to -100
CSF - 0
GREY MATTER - 32 - 41
WHITE MATTER - 23 - 34
ACUTE BLOOD - 56 - 76
CALCIFICATION - 60 - 400
BONE - 1000