You are on page 1of 11


Interhemispheric Fissure Central sulcus

• Hugely deep (down to the corpus callosum Paracentral sulcus
• Divides brain into 2 hemispheres Post central sulcus

Sylvian fissure
• Hugely deep
• Mostly horizontal
• Insula is buried within it
• Separates tempral lobe from parietal and
frontal lobes

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

Cingulate Sulcus STROKE

• Divides the gingulate gyrus from precuneus 2 major types:
and paracentral lobule • 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
- MCC is trauma
- In absence of trauma: due to
- Manifestations: severe H/A,
seizure, LOC
- Increase in density in area of
• Ischemic stroke

**Serpiginous: AV Malformation

• 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

Coagulopathy related Intracerebral Hemorrhage

• Can be due to drugs such as Coumadin or a
systemic abnormality such as
• On imaging:
o Heterogeneous appearance due to
completely clotted blood
o A fluid level within a hematoma
Intracerebral Hemorrhage suggests coagulopathy as an
• Causes underlying mechanism
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

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
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

Subarachnoid hemorrhage
• Most common cause- ruptured cerebral • The detached clot often originates from the
aneurysm heart or from the walls of large vessels such as
• Cerebral aneurysms are frequently located the carotid arteries
around the Circle of Willis • Atrial fibrillation is also a common cause
• Common aneurysm locations: ACoA, PCoA, • Account for 30% of all strokes
MCA bifurcation, tip of the basilar artery
• Typically presents as the “worst headache of Lacunar infarction
life” • Occurs when the walls of the small arteries
• The re-hemorrhage rate of ruptured aneurysms thicken
is high and often fatal • Cause the occlusion of the artery
• On CT: • Typically involve the small perforating vessels
o Appears as high density within sulci of the brain and result in lesions that are less
and cisterns than 1.5 cm in size
o The insular regions and basilar cisterns
o May have associated intraventricular Hypoperfusion Infarction
hemorrhage and hydrocephalus • Occur under two circumstances
o Global anoxia may occur from cardiac
or respiratory failure
o Presents an ischemic challenge to the
• 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
ISCHEMIC STROKE o Loss of insular ribbon
o Loss of gray white distinction
• Caused by blockage of flow in a major cerebral
o Sulcal effacement
blood vessel due to a blood clot
• Account for about 84% of all strokes Notes:
• Further subdivided based on their etiology: Plain CT: can visualize hemorrhage of infarction
o Thrombotic stroke If shows dense basilar or MCA: signifies
o Embolic stroke infarction
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. Lentiform Nucleus Obscuration
• Account for 53% of all strokes • Due to cytotoxic edema in the basal ganglia
• This sign indicates proximal MCA occlusion,
Embolic stroke
which results in limited flow to the
• Occurs when a detached clot flows into and lenticulostriate arteries
blocks a cerebral artery
• 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

• Hyperacute
• Acute
• 1-3 days
Arteriovenous Malformation
• 4-7 days
• MRI is the imaging study of choice for AVM
• 1-8 weeks
• Months to year
• Serpiginous high and low signal within
feeding and containing areas (depending on
***SEE TABLE ON LAST PAGE (HYPERACUTE AND 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
• 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 Acute Subdural Hematoma (white areas)
parenchymal, although subarachnoid
hemorrhage associated with ad=rterial
aneurysms also occur
o Seizures (25%)
o Mass effect, steal phenomenon
o Venous hypertension
o headache

Subacute Subdural Hematoma (similar density

as parenchyma)

Cavernous hemangiomas
• lobulated collections of dilated endothelial
lined sinusoidal spaces
• the most common vascular malformation in the
• 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 Chronic Subdural Hematoma (hematoma is
being fairly common similar to CSF)
o Contrast – enhancement of lesions is
• 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


Subdural Subdural hematoma

• Stretching or tearing of cortical veins CT
• Between dura and arachnoid • Acute
• Cross sutures but not dural attachments o Cresentric
• Frontoparietal convexities in the middle cranial o Hyperdense
fossa • Subacute
o Isodense
• Chronic • Rupture of a cerebral aneurysm – most
o Hypodense common cause in the absence of trauma
o Rehemorrhage o A large amount of subarachnoid
MRI hemorrhage. Particularly in the basilar
• Hyperacute cisterns
o T1- iso • On NECT
o T2- iso / hyper o Thin high density fluid collections
• Acute within the superficial sulci and CSF
o T1- iso / mod hypo cisterns
o T2- hypo o High density blood (fills the sulci over
• Subacute the right cerebral convexity)
o T1 and T2- hyper
• Chronic
o T1- iso / hypo
o T2- hyper

• Associated with a skull fracture
• Lacerated meningeal arteries
• Between skull and dura
• Cross dural attachments but not sutures
• Temporoparietal area

Secondary Effects of Craniocrebral Trauma

• Cerebral herniations
• Traumatic ischemia, infarction secondary (to)
• Diffuse cerebral edema
• Hypoxic injury

• On CT
o Biconvex
o Displaced gray-white matter CEREBRAL HERNIATIONS
o 2/3 hyperdense • Subfalcial (cingulate) herniation
o 1/3 mixed hyper / hypo • Uncal herniations
• On MRI • Transtentorial herniation
o Biconvex
• External herniation
o T1- iso
• Tonsillar herniation
o 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
o Subcortical white matter
Diffuse Axonal Injury o Posterior limb internal capsule
• Is often referred to as “shear injury” o Corpus callosum
• Most common cause of significant morbidity in o Dorsolateral midbrain
CNS trauma o The dorsolateral brain stem
• 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 Notes:
• Non hemorrhagic injuries are better shown on Intracerebral hemorrhage 20 to trauma:
T2 weighted images as hyperintensities 1. DAI
• Most common locations 2. Cerebral contusion (MC location: temporal
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 • Conforms to the shape of the cerebral
with foci of hemorrhage hemisphere
o Adjacent subarachnoid hemorrhage is • Chronic with rebleeding
o After 24-48 hrs, hemorrhagic
transformation or coalescence of
petechial hemorrhages into a rounded

Epidural Hematoma

Subdural Hematoma

• Biconvex
• Acute, contusion hematoma
• 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 spaces-
suprasellar and perimesencephalic
Multiple Petechial Hemorrhage in Diffuse Axonal (ambient, and quaadrigeminal plate)
Injury cisterns
Infarct After 4-7 In 1-8
(<12hrs) 1-3 days days weeks Months - Year
CT normal (50- increasing gyral mass
Scan 60%) mass effect enhancem effect
ent- due to resolves
of the BBB,
of the
brain tissue
hyperdense wedge persistent enhance
artery shape low mass effect ment may
density persist
obscuration of hemorrhagi
the lentiform c
nucleus transformati
on T1 sulcal
wt effacement
loss of gray-
white matter
Acute Infarct (12hrs- 1-3 days 4-7 days In 1-8 Months-Year
24 hrs) weeks
CT low density increase contrast volume loss
Scan basal ganglia mass effect enhancem
loss of gray- wedge mass encephalomala
white matter shape low effect cic change
interface density area resolves
involves the
gray white
sulcal hemorrhagi
effacement c
MRI hyperdensity intravascula contrast encephalomala
on T2 r or enhancem cic change
meningeal ent
enhanceme persists
nt begins
menigeal early mass volume loss in
effacment parenchyma effect affected
adjacent to l CE resolves vascular
the infarct distribution
mass effect hemorrhagi decrease hemorrhagic
c abnormal residua
transformati signal on
on T2
c changes
evolve and
In a 70 y/o man, the lateral ventricles and sulci are also
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

Review by Dra:
1. With presentation of LOC, the first modality to
order is CT scan to rule out infarct or
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
- 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


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