NEURORADIOLOGY
Interhemispheric Fissure

Hugely deep (down to the corpus callosum

Divides brain into 2 hemispheres
Central sulcus
Paracentral sulcus
Post central sulcus
Sylvian fissure

Hugely deep

Mostly horizontal

Insula is buried within it

Separates tempral lobe from parietal and frontal lobes
Notes:
Diffusion weighted images (DWI): important in increasing density in
areas with acute infarct
MRI: depicts more of the brain anatomy (in that case, better than
CT)
Most common location of Hypertensive plane: area of thalamus
Cingulate Sulcus

Divides the gingulate gyrus
paracentral lobule
from
precuneus and
STROKE
2 major types:

Hemorrhagic stroke
a. Intracerebral: due to drugs like Coumadin (warfarin)
or due to thrombocytopenia
b. SAS: due to rupture of cerebral aneurysm as a result
of hypertension bleed (affects basal ganglia) and
amyloid coagulopathy
Pathognomonic of Coagulopathy: fluid level with
blood
SAS:
MCC is trauma
In absence of trauma: due to cerebral
aneurysm
Manifestations: severe H/A, seizure, LOC
Increase in density in area of cistern

Ischemic stroke
**Serpiginous: AV Malformation
HEMORRRHAGIC STROKE



Are due to a rupture of a cerebral blood vessel that causes
bleeding into or around the brain
Accounts for 16% of all strokes
2 major categories of hemorrhagic stroke
o Intracerebral hemorrhage
– the most common, accounts for 10% of all
strokes
o
Subarachnoid hemorrhage
– due to rupture of a cerebral aneurysm,
accounts for 6% of strokes overall
Intracerebral Hemorrhage

Causes
o Hypertensive hemorrhage- most common cause
of non traumatic intracerebral hematoma
o Other causes: amyloid angiopathy- a ruptured
vascular
malformation,
coagulopathy,
hemorrhage into a tumor, venous infection, and
drug abuse
Hypertensive hemorrhage

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 poor prognosis

Commonly due to vasculopathy involving the deep
penetrating arteries of the brain

Has a predilection for deep structures including the
thalamus, pons, cerebellum, and basal ganglia—
particularly the putamen and external capsule
Coagulopathy related Intracerebral Hemorrhage

Can be due to drugs such as Coumadin or a systemic
abnormality such as thrombocytopenia

On imaging:
o Heterogeneous appearance due to completely
clotted blood
o A fluid level within a hematoma suggests
coagulopathy as an underlying mechanism
Hemorrhage due to Arteriovenous Malformation

Underlying arteriovenous malformation (AVM) may or
may not be visible on a Ct scan. However, prominent
vessels adjacent to the hematoma suggest an underlying
AVM. In addition, some AVM contains dysplastic areas of
calcifications and may be visible as serpentine enhancing
structures
Subarachnoid hemorrhage

Most common cause- ruptured cerebral aneurysm

Cerebral aneurysms are frequently located around the
Circle of Willis




Common aneurysm locations: ACoA, PCoA, MCA
bifurcation, tip of the basilar artery
Typically presents as the “worst headache of life”
The re-hemorrhage rate of ruptured aneurysms is high and
often fatal
On CT:
o Appears as high density within sulci and cisterns
o The insular regions and basilar cisterns
o May
have
associated
intraventricular
hemorrhage and hydrocephalus


Cause the occlusion of the artery
Typically involve the small perforating vessels of the brain
and result in lesions that are less than 1.5 cm in size
Hypoperfusion Infarction

Occur under two circumstances
o Global anoxia may occur from cardiac or
respiratory failure
o Presents an ischemic challenge to the brain

Tissue downstream from a severe proximal stenosis of a
cerebral artery may undergo a localized hypoperfusion
infarction
CT findings of Stroke

Presence or absence of hemorrhage

Dense MCA or dense basilar artery

Subtle changes of acute ischemia
o Obscuration of the lentiform nuclei
o Loss of insular ribbon
o Loss of gray white distinction
o Sulcal effacement
ISCHEMIC STROKE



Caused by blockage of flow in a major cerebral blood
vessel due to a blood clot
Account for about 84% of all strokes
Further subdivided based on their etiology:
o Thrombotic stroke
o Embolic stroke
o Lacunar stroke
o Hypoperfusion infarction
Thrombotic Stroke

Occurs when a blood clot forms in situ within a cerebral
artery and blocks and reduces the flow of blood through
the artery

May be due to an underlying stenosis, rupture of an
atherosclerotic plaque, hemorrhage within the wall of the
blood vessel, or an underlying hypercoaguable state

May be preceded by a transient ischemic attack and often
occurs at night or in the morning when the blood pressure
is low.

Account for 53% of all strokes
Embolic stroke

Occurs when a detached clot flows into and blocks a
cerebral artery

The detached clot often originates from the heart or from
the walls of large vessels such as the carotid arteries

Atrial fibrillation is also a common cause

Account for 30% of all strokes
Lacunar infarction

Occurs when the walls of the small arteries thicken
Notes:
Plain CT: can visualize hemorrhage of infarction
If shows dense basilar or MCA: signifies infarction
Lentiform Nucleus Obscuration

Due to cytotoxic edema in the basal ganglia

This sign indicates proximal MCA occlusion, which results
in limited flow to the lenticulostriate arteries

Lentiform nucleus obscuration can be seen as early as one
hour post
Diffuse Hypodensity and Sulcal Effacement

Most consistent sign of infarction

Extensive parenchymal hypodensity is associated with
poor outcome

If this sign is present in greater than 50% of the MCA
territory there is, on average, an 85% mortality rate
CERBRAL INFARCTION






Hyperacute
Acute
1-3 days
4-7 days
1-8 weeks
Months to year
***SEE TABLE ON LAST PAGE (HYPERACUTE AND ACUTE INFARCT)
INTRACRANIAL HEMORRHAGE
INTRACRANIAL VASCULAR MALFORMATION
Arteriovenous Malformation

MRI is the imaging study of choice for AVM detection

Serpiginous high and low signal within feeding and
containing areas (depending on flow rates) is seen in all on
MR/ MRA

Adjacent parenchymal atrophy may be present secondary
to vascular steal and ischemia

Brain parenchymal is replaced, but not displaced

Edema is present only with recent hemorrhage or venous
thrombosis and infarction

Four anatomic components
o Arterial feeders
o Arterial collaterals
o Nidus
o Venous outflow

Causes
o Hemorrhage (50%) – most are parenchymal, although
subarachnoid hemorrhage associated with ad=rterial
aneurysms also occur
o Seizures (25%)
o Mass effect, steal phenomenon
o Venous hypertension
o headache
Cavernous hemangiomas

lobulated collections of dilated endothelial lined sinusoidal
spaces

the most common vascular malformation in the brain

90% are supratentorial with the frontal and temporal lobes
(deep white matter, corticomedullary junction and basal
ganglia) being the most frequently involved sinus



Presentation is usually between 20 and 40 years of age
and more than 50% of the time, the lesions are multiple
On CT:
o Non contrast – isodense to moderately
hyperdense lesions with calcifications being
fairly common
o Contrast – enhancement of lesions is variable
On MRI:
o On T1 wt – the classic lesion has mixed signal or
“popcorn-like” core that is surrounded by a low
signal hemosiderin rim. The mixed signal of
“popcorn-like” core is the result of hemorrhage
in different stages of evolution
CRANIOCEREBRAL TRAUMA
Subdural

Stretching or tearing of cortical veins

Between dura and arachnoid

Cross sutures but not dural attachments

Frontoparietal convexities in the middle cranial fossa
Acute Subdural Hematoma (white areas)
Subacute Subdural Hematoma (similar density as parenchyma)
Chronic Subdural Hematoma (hematoma is similar to CSF)
Subdural hematoma
CT

Acute
o Cresentric
o Hyperdense

Subacute
o Isodense

Chronic
o Hypodense
o Rehemorrhage
MRI

Hyperacute
o T1- iso
o T2- iso / hyper

Acute
o T1- iso / mod hypo
o T2- hypo

Subacute
o T1 and T2- hyper

Chronic
o T1- iso / hypo
o T2- hyper
Epidural





Associated with a skull fracture
Lacerated meningeal arteries
Between skull and dura
Cross dural attachments but not sutures
Temporoparietal area


On CT
o
o
o
o
On MRI
o
o
o
CEREBRAL HERNIATIONS
Biconvex
Displaced gray-white matter
2/3 hyperdense
1/3 mixed hyper / hypo





Subfalcial (cingulate) herniation
Uncal herniations
Transtentorial herniation
External herniation
Tonsillar herniation
Biconvex
T1- iso
Displaced dura seen as thin, low signal line
between hematoma and brain
Subarachnoid hemorrhage (ang gulo ng arrangement ni dra.)

Occurs with injury of small arteries or veins on the surface
of the brain

The ruptured vessel bleeds into the space between the pia
and arachnoid matter

Trauma- most common cause
o Occurs most commonly over the cerebral
convexities or adjacent to otherwise injured
brain

Rupture of a cerebral aneurysm – most common cause in
the absence of trauma
o A large amount of subarachnoid hemorrhage.
Particularly in the basilar cisterns

On NECT
o Thin high density fluid collections within the
superficial sulci and CSF cisterns
o High density blood (fills the sulci over the right
cerebral convexity)
Diffuse Axonal Injury

Is often referred to as “shear injury”

Most common cause of significant morbidity in CNS
trauma

50% of all primary, intra-axial injuries are diffuse axonal
injuries

Mechanism: sudden deceleration or angular acceleration
causing shear strain injuries

Marked neurological impairment disproportional with CT
finding with a normal CT is typical

CT suggests DAI if petechial hemorrhages are found

MRI can be useful in demonstrating the extent of injury

T1 wt images will show hemorrhages as hyperintensities

Non hemorrhagic injuries are better shown on T2
weighted images as hyperintensities

Most common locations
o Subcortical white matter
o Posterior limb internal capsule
o Corpus callosum
o Dorsolateral midbrain
o The dorsolateral brain stem
Secondary Effects of Craniocrebral Trauma

Cerebral herniations

Traumatic ischemia, infarction secondary (to) hemorrhage

Diffuse cerebral edema

Hypoxic injury
Notes:
Intracerebral hemorrhage 20 to trauma:
1. DAI
2. Cerebral contusion (MC location: temporal lobe)
Cerebral Contusion

The most common primary intra-axial injury

Often occur when the brain impacts an osseous ridge or a
dural fold

The foci of punctuate hemorrhage or edema are located
along the gyral crests

On CT:
o An ill defined hypodense area mixed with foci of
hemorrhage
o Adjacent subarachnoid hemorrhage is common
o After 24-48 hrs, hemorrhagic transformation or
coalescence of petechial hemorrhages into a
rounded hematoma
Epidural Hematoma


Biconvex
Acute, contusion hematoma
Multiple Petechial Hemorrhage in Diffuse Axonal Injury
Subdural Hematoma



Conforms to the shape of the cerebral hemisphere
Chronic with rebleeding
Similar to MS (has on and off sxs); the difference is there is
a history of trauma in DAI
Cerebral Edema

Most life threatening

Most reliable early imaging finding:
o Effacement of the surface sulci and basilar
subarachnoid
spacessuprasellar
and
perimesencephalic
(ambient,
and
quaadrigeminal
plate)
cisterns
Infarction
CT Scan
Hyperacute
Infarct (<12hrs)
normal (50- 60%)
1-3 days
increasing
mass effect
After 4-7 days
gyral
enhancementdue to the
breakdown of
the BBB,
neovascularity,
reperfusion of
the damaged
brain tissue
In 1-8 weeks
mass effect
resolves
hyperdense
artery
wedge shape
low density
persistent
mass effect
enhancement
may persist
obscuration of
the lentiform
nucleus
hemorrhagic
transformation
4-7 days
In 1-8 weeks
Months - Year
MRI
on
wt
T1
sulcal effacement
gyral effacement
loss of gray-white
matter interface
Acute Infarct (12hrs-24 hrs)
CT Scan
Months-Year
low density basal
ganglia
increase mass
effect
contrast
enhancement
persists
volume loss
loss of gray-white
matter interface
wedge shape
low density
area that
involves the
gray white
matter
hemorrhagic
transformation
mass effect
resolves
encephalomalacic
change
intravascular
or meningeal
enhancement
begins
decreasing
early
parenchymal
CE
contrast
enhancement
persists
encephalomalacic
change
mass effect
resolves
volume loss in
affected vascular
distribution
hemorrhagic
transformation
decrease
abnormal
signal on T2
hemorrhagic
changes
evolve and
become
chronic
hemorrhagic
residua
sulcal effacement
MRI
1-3 days
hyperdensity on
T2
menigeal
effacment
adjacent to the
infarct
mass effect
Notes:
In a 70 y/o man, the lateral ventricles and sulci are also prominent
MRI: CSF – white on T2 weighted
Black on T1
Enhancement of ________: T1 weighted with contrast
DWTI: Blurred image
Loss of gray and white matter interface:
 If white and without contrast enhancement – acute
infarct
 With contrast enhancement – subacute infarct
Review by Dra:
1. With presentation of LOC, the first modality to order is CT
scan to rule out infarct or hemorrhage
2. In acute infarct, common finding is a dense basilar or MCA
(most common)
3. Observe the lentiform nucleus
- If there is obliteration, then it is acute infarct
- If it has a normal finding, it is a hyperacute infarct.
Repeat CT scan after 1 day.
In hyperacute infarct:
a. aside from the normal CT, you also see a hyperdense
artery and obliteration of the lentiform nucleus
b. MRI (T1 weighted): gyral edema and loss of gray-white
matter interface
After 1-3 days: CT shows increase mass effect and wedge-shaped
Subacute: hypodense (darker than adjacent brain parenchyma),
meningeal enhancement, wedge-shaped, mass effect
Chronic: No mass effect, density of infarct similar to CSF, rebleeding,
meningeal enhancement
Bright on DWTI (blurred image): acute or hyperacute
1. Presence of white areas: acute infarct
2. If dark: look at the contrast
a. With enhancement of infarct: subacute
b. Similar to CSF: chronic
CT: blood is white; ischemia is similar to parenchyma
1. Look at the basal ganglia and thalamus
2. MCA