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NEURORADIOLOGY

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

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 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
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

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
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
abuse

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
capsule

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
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
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

CERBRAL INFARCTION
• Hyperacute
• Acute
INTRACRANIAL VASCULAR MALFORMATION
• 1-3 days
Arteriovenous Malformation
• 4-7 days
• MRI is the imaging study of choice for AVM
• 1-8 weeks
detection
• 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
ACUTE INFARCT)
• Adjacent parenchymal atrophy may be present
secondary to vascular steal and ischemia
INTRACRANIAL HEMORRHAGE
• 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 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
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 Chronic Subdural Hematoma (hematoma is
being fairly common similar to CSF)
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 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

Epidural
• 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)
hemorrhage
• 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
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 • Conforms to the shape of the cerebral
with foci of hemorrhage hemisphere
o Adjacent subarachnoid hemorrhage is • Chronic with rebleeding
common
o After 24-48 hrs, hemorrhagic
transformation or coalescence of
petechial hemorrhages into a rounded
hematoma

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
Infarction
Hyperacute
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
the
breakdown
of the BBB,
neovascular
ity,
reperfusion
of the
damaged
brain tissue
hyperdense wedge persistent enhance
artery shape low mass effect ment may
density persist
obscuration of hemorrhagi
the lentiform c
nucleus transformati
on
MRI
on T1 sulcal
wt effacement
gyral
effacement
loss of gray-
white matter
interface
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
ent
persists
loss of gray- wedge mass encephalomala
white matter shape low effect cic change
interface density area resolves
that
involves the
gray white
matter
sulcal hemorrhagi
effacement c
transformati
on
MRI hyperdensity intravascula contrast encephalomala
on T2 r or enhancem cic change
meningeal ent
enhanceme persists
nt begins
decreasing
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
hemorrhagi
c changes
evolve and
become
chronic
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