adiuvante Dei gratia doctorum factionis 2014-2015

RADIO: Neuro Dr. Ragunjan

In evaluating the brain you have to
INTRODUCTION - First to see the midline, the symmetry of the right and left
Always check for Symmetry! side
- Evaluate the cisterns, ventricles and basal structures
BASAL CISTERNS
 Quadrigeminal plate cistern – appearance of a symmetric RADIOGRAPHY
smile
 Usually requested in the emergency in a patient who had
 Suprasellar cistern – like a pentagon trauma, maybe secondary to fall or a vehicular accident. Able to
show fractures
MODALITIES USED in CNS EXAMINATION  In a normal xray of the skull taken on the side, you will be able
to appreciate the coronal suture. If there is another suture there
1. Ultrasound then that’s pathological→ probably a fracture
2. CT Scan
 Acute neurologic illness (24-48hrs)
3. Angiography
 Primary vascular lesion (AVM)
4. Radionuclide (nuclear imaging)
5. Magnetic resonance (MR)
 Chronic & subacute cases (>2days)

 Adult Skull
 Skull approximates face
 Child Skull
 Skull is bigger in comparison with the face

ANALYSIS CRANIAL ULTRASOUND

 Mass – displacement of normal structures away form  Used in neonates, uses a special type of probe
abnormality  Able to take coronal, axial and sagittal view
 Atrophy – widening of ipsilateral sulci or enlargement of  R and L side must be symmetrical
the ventricle adjacent to the lesion
 Mass Lesion CRANIAL CT-SCAN
o Intra-axial – w/in the brain and expanding it
 Metastases  Choice for the evaluation after acute trauma
 Intracranial Hemorrhage  suspected acute intracranial haemorrhage
 Primary intracranial tumor –  diseases of the skull base or calvaria
glioblastoma  has superior brain detail
 Brain abscesses  when MRI is contraindicated
o Extra-axial – outside & compressing it  Brain Window VS Bone Window
 Subdural/epidural hematoma  Brain Window →Enable to demonstrate the brain parenchyma
 Meningioma  Bone Window →shows bone detail
 Neuromas  If with contrast
 Cysts - Able to provide enhancement for
 Gray Matter or White Matter o Cisterns
o Gray Matter o Vessels
 Infarct, trauma, encephalitis o Choroid Plexuses
o White Matter
 Wide causes
 Traumatic lesions
o Contra-coup injury: lesion opposite the blow

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 MRI - No tedious pre-diagnostic preparations needed
- Injects 2 bottles of contrast and start scanning
 Shows multiplanar images
 Has outstanding soft tissue resolution
 Primarily used for the brain MR Angiography
 Absence of radiation - Done without contrast
 Cannot demonstrate bone detail and calcification and long - Relies on blood flow within the vessels
imaging time is required - May also be done with contrast→ better image quality

C/I INTRACRANIAL ABNORMALITY ANALYSIS

- In patient who has pacemakers and other metal implants
Extra VS Intraparenchymal ?
MR Spectorscopy Simple or Multiple?
- A recent softeware in MRI Whithin gray or white matter?
- Able to compute different metabolite like choline, Any atrophic changes?
aspartate creatine and lactic acid. - Reversible / irrebersible?
- Able to differentiate between tumor, abscess, gliosis or Location
infarction - Cerebrum
- Cerebellum
Diffusion Weighted Imaging - Brainstem
- The only protocol in MRI that is able to detect
hyperacute to acute infarct Reaction to contrast enhancement
- Shows area of ischemia in < 6 hours - Highly Enhancing?
- - Moderately Enhancing?
REASONS for the USE of IV CONTRAST - Poor Enhancing?

 Iodinated contrast (for CT) and gadolinium paramagnetic contrast HEAD TRAUMA
(for MR) do not cross the blood brain barrier
 In the presence of pathology/ disruption of the BBB, contrast will
CT-Scan→ Diagnostic method of choice for acute head trauma
localize in the site of pathology - UCT scan is also used in imaging of hemorrahage
 Also improves definition of vascular and dural structures - Quick, widely available and highly accurate
 When you are suspecting for a tumor - Able to detect fractures
o Iodinated Gadolinium for CT Scan
o Paramagnetic for MRI CT is the diagnostic method of choice; MRI slowly supplanting CT
o If there is enhancement likely
- detection of hemorrhages – subarachnoid,
the BBB is disrupted →Tumor
intraparenchymal, extraaxial (subdural, epidural)
 Defines circle of willis for possible aneurysm
- contusions, diffuse axonal (shearing) injury, diffuse brain
swelling
X-RAY & ULTRASOUND

 x-ray has no meaningful role

 ultrasound has limited use because of thick calvaria
 in neonates and infants, use the open fontanels
 transcranial doppler probes for intracranial evaluation
o if you are thinking of a vascular anomaly in a newborn

ANGIOGRAPHY & RADIONUCLIDE IMAGING

 Used to look for any vascular abnormality

o CT Angiography
o MR Angiography
 Radionuclide Imaging
o Used in seizure disorders, dementia, psychiatric
disorders and brain death Black Arrow→ Air possible secondary to laceration
MRI→ not used in acute trauma
Digital Subtraction Angiography - modality of choice in subacute and chronic
- Previously used, where in they cannulated the femoral hematomas [ Hemahtoowmaz ]
artery→places catheter in the ICA→injects contrast - requested if with equivocal CT-Scan result
→multiple images will be shot→ monitors shows the image Skull X-Ray
- Invasive procedure - not that helpful because you will only see fractures, you
o Needs a lot of procedure and clearance prior will not be able to tell whether is it intra or extracranial
Cerebral CT Angiography
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 PNEUMOCEPHALUS Extraaxial
- Epidural Hemorrhage
 Depressed Fractures - Subdural Hemorrhage
 air within the cranium - Subareachnoid Hemorrhage
 air in CT →Black - Intraventriclar Hemorrhage
 Maybe secondary to disruption of frontal sinuses, mastoids or a Intraaxial
linear fracture - Within the parenchyma
BONE FRACTURES - Diffuse Axonal Injury
- Cortical Contusions
 Nondisplaced linear fractures – MOST COMMON - Intracerebral Hematoma
- Subcortical
TEMPORAL BONE FRACTURE - Vascular Injury

 may present w/ deafness, facial nerve palsies, vertigo, dizziness, PRIMARY HEAD INJURY – EXTRA-AXIAL
or nystagmus EPIDURAL HEMATOMA
 Physical signs : ecchymosis over the mastoid process (“Battle
sign”)  Arterial in origin, result from skull fracture→ rupture that
 Transverse Temporal Bone Fracture disrupts the middle meningeal artery of the MCA
o A liner or lucent area traversing the  Hematoma strips the dura → ovoid mass displaces adjacent
petrous portion of the temporal bone brain
(perpendicular)  Skull fractures in 85-95%
o Usually from a blow to occiput or frontal  On CT/MRI→
region
o Complications: sensorineural hearing loss  Lenticular in shape , high attenuation, Biconvex,
Extraaxial collection
 Do not cross cranial suture kasi nasa taas sya ng dura
(periosteal layer of dura is firmly attached)
 May cross midline because they are external to the falx
 MOST are temporal or temporoparietal in location,
 most commonly occur in the lateral surface of cerebral
hemisphere
 hyperacute hematoma - first hour of injury
 portions of low density blood indicating bleed has not yet
clotted or is still bleeding; neurosurgical emergency!
 acute hematoma - 1 to 2 hours
 hyperdense (but may be hypodense in px with anemia or
DIC)
 if hypodense hindi pa nag cla clot, meaning actively
bleeding yung site Emergency!!
 Longitudinal temporal Fracture  occur between the dura and calvaria – constrained; resulting in
o Fracture is parallel to the petrous bone biconvex configuration
o Sensorineural hearing loss uncommon
 Mix
 Prior to identifying fracture and where they are, you must have a
good anatomic picture of the brain

HEAD INJURY

Primary
- Occurs as a direct result of the blow to the head
- Epidural, subdural, subarachnoid, & intraventricular Hge,
DAI, cortical contusions, intracerebral hematomas, &
subcortical gray matter injury
Secondary
- Often preventable
- Consequence of primary lesion
o Vascular compromise or mass effect
- Cerebral swelling, brain herniation, hydrocephalus,
ischemia or infarction, CSF leak, leptomeningeal cyst, and
encephalomalacia

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 SUBDURAL HEMATOMA

 Venous in origin, stretching or rupture of cortical veins that

traverse the subdural space en route (LJ special mention ka dito!
Haha) to the dural sinuses
 Extends on a much larger area than epidural (bec. they are not as
firmly attached)
 Commonly after acute deceleration injury from a motor vehicle
accident or fall. SUBARACHNOID HEMORRHAGE
 Crescent Shape
 Most are supratentorial, located along the convexity  disruption of small subarachnoid vessels or direct extension into
 Cross Sutural Margins the subarachnoid space by a contusion or hematoma.
 Diffuse swelling of underlying hemisphere common  CT: linear areas of high attenuation w/in the cisterns & sulci
 Displaced cortex with white matter buckling, midline shift, &  Differentiated from subdural hematomas by extension into
thick gray matter mantle adjacent sulci
 MRI detects small subdural hemorrhages  Maybe secondary to ruptured aneurysm rather than trauma as
o Sometimes missed on CT Scan primary cause
 May have a marked mass effect on the underlying brain tissue  May lead to hydrocephalus by impaired CSF resorption at the
 May be able to see hematocrit effect or layering on the site of level of arachnoid villi
subdural hematoma  Subarachnoid Spaces
- Arrow: Layering→maybe due to active bleeding o Within cortical sulci and gyri
( Hematocrit Effect ) seen in patients w/ clotting o Interhemispheric falx
disorders or in patients w/ rebleeding into an older
subdural collection o Cisterns
o Lateral fissures
 If nag pooled na sya sa basal part→ white areas within cisterns

- hyperdense, isodense, hypodense

o hyperdense in early stage - 1 to 10 days
o isodense - 1 to 3 weeks
o hypodense - after 1 month
- crescentic configuration
- mass effect is greater than the size of the hematoma;
reflect underlying brain swelling and injury that
accompanies the hematoma

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 INTRAVENTRICULAR HEMORRHAGE  More hemorrhagic than DAI
 Common site
 Result from o Temporal lobe above petrous bone
st
1 : rotationally induced tearing of subependymal veins on the o Posterior to the greater wing of sphenoid
surface of the ventricles. o Frontal lobes along the cribriform plate
nd
2 : direct extension of a parenchymal hematoma into the ventricular o Planum sphenoidale & lesser sphenoid wing
system.  CT Findings
rd
3 : intraventricular blood can result from retrograde flow of o Areas of hypodensities → Edema
subarachnoid hemorrhage into the ventricular system through the o Areas of hyperdensities→ Hemorrhage → Salt and
fourth ventricular outflow foramina. pepper pattern
 CT: hyperdense, layering dependently w/in ventricular system o During the 1st week, areas of hypodensity &
 May resul to irritation of the ependymal lining of the ventricles hyperdensity (“salt & pepper” pattern)
→Hydrocephalus may set in  MRI
 Poorly marginated areas with gyral morphology in the temporal
PRIMARY HEAD INJURY – INTTRA-AXIAL and frontal lobes
DIFFUSE AXONAL INJURY  Nasa cortical superficial gray mater, medyo outer area of the
brain
 In severe head trauma, high speed motor vehicle crashes  White with surrounding black sa frontal and temporal lobes
 White→ Hge
 LOC starts immediately after injury
 Black →Edema
 widespread disruption of axons that occurs at the time of an
acceleration or deceleration injury. INTRACEREBRAL HEMATOMA
 Affected areas may be distant, direct impact is NOT necessary
 Better seen in MRI than CT scan  Shear induced haemorrhage from rupture of small
intraparenchymal vessels, less surrounding edema than cortical
contusions
 MOST are located in frontotemporal White Matter
 MRI  Inside the brain parenchyma
 Usually located in the basal ganglia or temporal region
 Small petechial hemorrhages at the gray–white junction of
 MRI → Hematoma + edema surrounding it
the cerebral hemispheres or corpus callosum that may
persist for years
 Depending on the protocol→ maybe seen as gray white
mater petechial hemmorages
 There is disruption of the neurons due to sudden acceleration or
deceleration
 CT
 Petechial hemorrhages within gray white mater junction
 White Matter → Black sa CT Scan (decreased attenuation)

SUBCORTICAL GRAY MATTER INJURIES

 Multiple petechial hemorrhages particularly affecting the basal ganglia

and thalamus
 Microscopic perivascular collection of blood from rupture of small
perforating vessels

VASCULAR INJURIES

 ICA is usually involved, most commonly injured (at sites of fixation)

 Entrance to carotid canal at the base of petrous bone
 As it exit from cavernous sinus below anterior clinoid process
 MR: Intramural hemotoma
CORTICAL CONTUSIONS  Carotid Cavernous Fistula - communication between the cavernous
portion of the internal carotid artery and the surrounding venous
 Areas of focal brain injuries primarily involving the superficial gray mater plexus.
 Much less likely to have LOC  Clinically → bulging proptosed eye, enlargement of EOM Uni o bi
 Better prognosis than DAI lateral (usually bilateral because venous channels connect the
 Common in Px w/ severe head trauma, well seen on CT cavernous sinuses)
 Occur near bony protuberances  Pulsating because of the communication of ICA with superior
ophthalmic vein
 Maybe multiple and bilateral
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  Dural Fistula: laceration of the middle meningeal artery o Causes focal effacement of ambient cistern and
lateral aspect of suprasellar cistern
o Kernohan Notch
 Focal impression on the cerebral
peduncle
 Mass effect on CN III (blown pupil w/
ipsilateral hemiparesis)
 Compression of contralateral cerebral
peduncle
Transtentorial
- Brain herniation either up or downward
Extrenal Herniation
o Herniation of brain parenchyma outside calvarium
Tonsillar
- Displacement of cerebellar tonsils into the cranio-
cervical junction

SECONDARY HEAD INJURIES

Diffuse Cerebral Swelling

- Occur either bec. Of increase cerebral blood volume or an
increase in tissue fluid content
- Effacement of sulci and compression of ventricular system
- Cerebral swelling: Due to hyperemia (inc. blood volume)
common in children & adolescents
- Diffuse cerebral edema: secondary to tissue hypoxia
- Cerebellum & brainstem usually spared (appear
hyperdense)

- May lead to brain herniation

- Secondary to mass effect produced by primary intracranial Hydrocephalus
injury - impaired CSF reabsorption or or obstruction at the level of
- Di na Makita yung ventricles the aqueduct or fourth ventricular outflow foramina.
- If there is a hematoma like in the left parietal area→ can push
the adjacentparenchyma leading to→ Subfalcine or cingulate
- Can occur after
gyrus herniation
o Subarachnoid hemorrhage
o CT
o Intraventricular hemorrhage
 Decreased attenuation
- With ventricular dilatation
 Loss of gray-white differentiation
- Can also be due to mass effect from cerebral swelling by
obstruction of drainage
Brain Herniation
- Subflacine
Ischemia / Infarction
o Cingulate gyrus is displaced across midline under
- Can result from:
flax cerebri
o Increased ICP
o Most common
o If there is a midline shift into the o Embolization from a vascular dissection
contralateral side underneath the falx o Direct Mass Effect
o Compression of adjacent lat. Ventricle, - Patterns
enlargement of contralat. Ventricle from o ACA Infarction from Subfalcine Herniation
obstruction at level of foramen of Monro o PCA Infarction from Uncal Herniation
o Risk of ACA infarction o PIC Infarction from Tonsillar Herniation
- Uncal
o Medial temporal lobe displaced medially is CSF Leak
diplaced medially over the free margin of - Secondary to dural tears/fracture
tentorium - Occur after calvarial or skull base fracture
o Displacement of the uncus or medial temporal - CT with intrathecal contrast  for detailed anatomical
lobe downwards localization
- Clinically→ CSF rhinorrhea and otorrhea (subarachnoid
space to paranasal sinuses/disrupted tympanic
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 membrane) - Plain Films and CT
- Radionuclide cisternography – highly sensitive o Used to localize and confirm radio opaque
intracranial foreign bodies
Leptomeningeal Cyst - CT Scan
- Growing fracture o Leaded Glass and Metal  Hyperdense
- Due to traumatic dural tear  outpouching of arachnoid at o Wood  Hypodense
site of suture or fracture - Gunshot Wound  MOST COMMON CAUSE
- CT o Metallic fragment / bullet can cause significant
o Lytic Skull Defect with scalloped margins streak artifact which may obscure underlying
injury  tilt the CT gantry to overcome this
problem 
o Bullet path is seen on CT as linear hemorrhagic
strip

- Complications: skull fractures, dural lacerations w/

resultant pneumocephalus, fragments that increase risk
for abscess formation
Encephalomalacia - Secondary Brainstem Injury – Duret hemorrhage: midline
- Tissue loss with surrounding gliosis from remote head hematoma in the tegmentum of the rostral pons and
injury midbrain in assoc. w/ descending transtentorial herniation
- Maybe symptomatic or a cause of seizure
- Related to: infarct, Hge, CHILD ABUSE
- CT - Non-accidental trauma – 80% deaths from head trauma in
o Low attenuation with volume loss children younger than 2 yrs of age
o Dilation of adjacent ventricles - Long bone fracture most common skeletal injury in child
- MR abuse
nd
o Follow CSF sequence except for gliosis - Skull fracture  2 most common skeletal injury in child
 Gliosis appears as increase signal abuse
intensity on proton densitiy and T2WI - CT
- Wallerian Degeneration o Done if with suspected intracranial injury
o Seen on CT especially MR Study - Subdural hematoma  MC intracranial complication of
o Are focal volume loss along white matter tracts child abuse
associated with cell death o Posterior interhemispheric fissure
o On CT  Hyperdense collection
- Whiplash Shaken Injury
o Subdural Hematoma
o Retinal Hemorrhage
o Metaphyseal Long Bone Fractures
- Shaken Impact Injury
o Coma
o Subdural hematoma
o Primary brain injury
- Diffuse Brain Swelling
o Most common intra-axial manifestation of
head injury related to child abuse
 Initial swelling associated with
vasodilation secondary to loss of
PENETRATING TRAUMA
autorgulation
- Penetrating Sharp Objects
- Damage is defined by the objects trajectory
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  At this stage injury might still  other causes - primary arterial diseases such as fibromuscular
be reversible hyperplasia, arterial dissections and arteritis; venous occlusive disease;
- Chronic Sequlae of head injury septic or tumor emboli
o Chronic Subdural Collection  CT most commonly employed
o Global Cerebral Atrophy  MRI is superior
o Encephalomalacia  CT scan findings depend on
 size of the abnormality
 association with significant hemorhage
 time interval between the time of infarct and the time of CT
scan
 location of the infarct

 CT scan finding may be normal within the first 24 hours if

nonhemorrhagic, small, or located in the brainstem
 infarcts involving the cerebral hemispheres are evident within the first
few hours after onset
 CT findings
 loss of distinction with the gray and white matter
CEREBROVASCULAR DISEASE  subtle obliteration of the cortical sulci
 reduced density related to vascular distribution
 STROKE  poorly defined, heterogeneous reduced density; may or may
 clinical term applied to any abrupt nontraumatic brain insult—
not cause mass effect
literally “a blow from an unseen hand.”
 caused by either brain infarction (75%) or hemorrhage (25%), and  may have sharp margin and homogeneous attenuation
must be distinguished from other conditions causing abrupt
neurologic deficits  MRI findings
 INFARCTION  demonstrates ischemic changes earlier than CT
 permanent injury that occurs when tissue perfusion is decreased  on T1-weighted images - decreased signal intensity with loss of
long enough to cause necrosis, typically due to occlusion of the normal signal difference between gray and white matter
feeding artery  on T2-weighted images - increased signal intensity
 TRANSIENT ISCHEMIC ATTACKS (TIAs)  small hemorrhages in the infarcts are seen on MRI but not seen
 defined as transient neurologic symptoms or signs lasting less on CT
than 24 hours, which may serve as a “warning sign” of an
infarction occurring in the next few weeks or months. HYPERTENSIVE HEMORRHAGES
 are often due to temporary occlusion of a feeding artery  often occur in the
 HEMORRHAGE  external capsule
 seen when blood ruptures through the arterial wall, spilling into  thalamus
the surroundingparenchyma, subarachnoid space, or ventricles.  internal capsule
 cerebellum
ISCHEMIC STROKE  pons
 lobar white matter
- Secondary to thrombi or emboli
seen in the putamen (35% to 50%)
- CT Scan is the most commonly employed kase available
subcortical white matter (30%),
kung saan saan pero for ischemia it is MRI daw talaga
cerebellum (15%),
- Take a look at the hyperdense artery sign
thalamus (10% to 15%), and
o Arteries should not be seen in plain CT Scan but if
pons (5% to 10%)
you see it then there must be an impending
infarct or ischemia within the distribution of that
 frequently rupture into the ventricular system
artery
o Acute Trauma / Hemorrhage→ CT Scan!!  areas of high density with sharply defined borders
- White because of stasis of blood  no edema in acute bleed; edema develops after several days
- MRI is superior  Small hypertensive hemorrhage may resolve with few deficits.
o If you don’t see a flow void→ thrombus→  poor prognosis
suspect infarct
 Bleeds in the posterior fossa, those with a large amount of mass
o MRI show you the ischemic part in <6 hours
- Insular ribbon sign effect
o + swelling in the insula  hemorrhages extending into the ventricular system
 Focal contrast extravasation within an acute hematoma on CTA or
CEREBRAL INFARCTION routine contrast-enhanced CT images (“spotsign”) predicts a high risk
 ischemic brain infarcts commonly due to atherosclerosis of clot expansion over the first several hours after admission compared
 embolic brain infarcts result from emboli from the heart withthose without a spot sign

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 CT Scan  junction between the internal carotid and posterior cerebral
- Loss of the tissue in the gray white mater interface artery
- Reduced density related to the vascular distribution  size from less than 1 mm to more than 5 cm
- ischemic brain infarcts commonly due to  those > 2.5 cm = giant aneurysm
atherosclerosis METASTASIS to the CNS from EXTRA-CRANIAL SITE
 embolic brain infarcts result from emboli from
the heart A cancer somewhere can spread to the brain. Either
 other causes - primary arterial diseases such as - Intraparenchymal lesions maybe seen from the o:
fibromuscular hyperplasia, arterial dissections o Lung Ca
and arteritis; venous occlusive disease; septic or o Breast Ca
o Melanoma
tumor emboli
o Colon Ca
- Extra axial pathologies will be prof
o Breast Ca
o Prostate Ca
o Lung Ca
Hyposensitivity o Neuroblastoma
- Hemorrhagic metastasis to the CNS maybe seen in
o Melanoma
Infarct on the o Renal Ca
R. ACA o Thyroid Ca
o Choriocarcinoma
CT- Scan
- Multiple foci in the gray-white mater junction and
are intensely enhancing
o Sometimes with leptomeningeal carcinomatosis
- Sometimes black/hypodense in plain scan
EDEMA - + enhancement in contrast enhanced CT
Cytotoxic MRI
- Intracellular - + enhancement in MRI with contrast
- Because of some cellular insult - Multiple lesions are scattered in the brain parenchyma
- Increased cell water content following the neuropathologic but maybe solitary in some of the cases
response to cell death
- Primarily a gray mater phenomenon Posterior Fossa Tumors
Maybe due to:
Vasogenic - Medullobastoma
- Extracellular - Pilocytic astrocytoma
- Related to loss of BBB - Ependymoma
- Disturbance in tight capillary junctions - Brainstem glioma
- Progress slowly and persists overt time
- Primarily a white mater phenomenon
Medulloblastoma
The most common pediatric CNS malignancy
INTRACRANIAL ANEURYSM - Located in the medulla
 dilatation of an artery
- Along with pilocytic astrocytoma is the most
 saccular/berry aneurysm - result of hemodynamic stresses common pediatric posterior fossa tumor
 other types - atherosclerotic, mycotic (infectious), posttraumatic
 become symptomatic because of rupture leading to subarachnoid and Pilocytic Astrocytoma
intraparenchymal hemorrhage
The other most common pediatric posterior fossa tumor aside
 suspected subarachnoid hemorrhage - do NECT (non-enhanced CT)
from Medullobalstoma
 unilateral location, above or below the tentorium gives evidence as to
- With cystic component
where the lesion is most likely located o May whitish component→ Cystic
→
SACCULAR ANEURYSMS - May result into a mass effect push adjacent structures
 very common, up to 5-9% of the adult population Ependymoma
 most aneurysms never rupture Are tumor in the ependymal lining of the ventricles
 once rupture occurs, 60% will either die or develop neurologic - Isodense with a mixture of calcification and cystic change
dysfunction - May occur sa kahit saang ventricle
 occur at points of major arterial branching Brainstem Glioma
 most common sites Causes Expansion of the brainstem
 proximal segment of middle cerebral artery - Sagittal view→ very good in imaging brainstem area
 anterior communicating artery

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 Meningioma
When we see the Dura, meningioma is there
Characteristics:
- Homogenously enhancing
- Supplied by dural arteries
- Has dural tails
- Obstruct sinuses

extraaxial tumors that arise from the arachnoid

- majority are benign
- common sites
o along superior sagittal sinus
o region of tuberculum sellae or anterior to the

tuberculum along the olfactory groove Intraventricular Tumors

o edge of sphenoidal ridge - Lobulated, whitish structures
o margin of falx cerebri and tentorium o Must be differentiated from haemorrhage, the
difference is that haemorrhage is no lobulated
- derive blood supply from arteries supplying the dura saka pag haemorrhage dapat nag po pool sa
o may parasitize vasculature of adjacent brain dependent portion
o may obstruct dural sinuses
o most incite osseous response (ie. hyperostosis) Pituitary Adenoma
and may invade bone producing hyperostotic Classified as hormonally active versus hormonally inactive
density on outer table - hormonally active adenomas are further subdivided
o may produce bone destruction according to the hormone they secrete
o some completely destroys bone, with a soft-tissue - depending on size , classified as
mass bulging externally o macroadenoma (>1cm)
o calcification found in 15-20% o microadenoma (<1cm)
o small punctate densities
o sand-like deposits = psammoma bodies - macroadenomas, usually hormonally inactive, become
o some form densely calcified masses clinically manifest as a result of their size, compressing
o homogeneous enhancement on contrast adjacent neural structures (ie. optic chiasm)
administration, with well defined margin and with
an adjacent dura tail - microadenomas seek medical attention because of
- MR shows hypointense lesion (T1W) and hyperintense abnormal hormone secretion
(T2W), with sharply defined magins o prolactinomas - galactorrhea and amenorrhea;
hypogonadism in male
o growth-hormone-secreting adenomas - gigantism;
acromegaly
o + alteration I the upper margin of the gland with
erosion of the sella
Dural - ACTH-secreting adenomas - Cushing’s disease
Tail
Pituitary Macroadenoma
- contrast MR - marked homogeneous enhancement
- cystic or necrotic areas in large macroadenomas

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 Craniopharyngioma - eighth cranial nerve most frequently involved; fifth
Congenital tumor which arises from remnants of Rathke’s Pouch nerve also
- tumor of childhood and adolescence - of the VIII CN - hearing loss, tinnitus, vertigo or dizziness
- In young children, clinical complaints are related to - most common tumor of the cerebellopontine angle
increased intracranial pressure - CT - large lesions will obliterate the CP angle, displace
- In older children and adults, symptoms are visual or brainstem and IV ventricle, and widen the contralateral
endocrine in nature (ie. Delayed growth) CP angle cistern
- Calcification occurs in 80% - small lesions may only enlarge the internal auditory canal
- most are suprasellar; 10-15% within the pituitary fossa - enhances considerably on contrast
- cystic changes may occur - MR - reduced signal on T2W; intense enhancement
- variable appearance on MR depending on the amount on contrast
of calcification (low intensity on T1w and T2W) and
cystic change (high signal on T1W and T2W) CNS Infection
- solid portions of the tumor enhance in a homogeneous Bacterial, Fungal, Viruses, Parasites and ____
manner
Present as large cyst-like sellar or supra sellar mass Pyogenic Cerebritis and Abscess
- with enhancement and calcifications - Early Cerebritis
- with soft tissue component on MRI - Late Cerebritis
- Early Capsule Stage
- Late Capsule Stage
- May come from direct extension secondary to trauma
[ Truhmuh HAHA
- Thru hematogenous route

- cerebritis/encephalitis
- most frequently from hematogenous dissemination
of infectious agents, often from the lung
- direct extension from sinuses or middle ear
- none produce totally characteristic radiographic finding
- immunosuppression, cyanotic heart disease, pulmonary
AV fistula predispose patients to develop brain abscess
- initially consist of small, scattered foci of cerebritis
- mature into well-demarcated, encapsulated lesion
- central portion with suppurative material and debris
-
- previously called neuromas or neurilemmomas which are
misleading
- adults; 2W:1M
CT - areas of hypodensities, with little enhancement on contrast
- later, neovascularity and collagen capsule develop; ring
enhancement become apparent

Craniopharyngioma with
necrosis

Schwannoma
- benign tumors occuring along the course of cranial, spinal
and peripheral nerves
o hindi lang sya sa brain meron din sya sa labas ng
CNS
o the most commonly involved in the cranium are
the CN VIII and CN V
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 Subdural and Epidural Empyema
In cases of osteomyelitis of the skull, sinusitis, meningitis and
penetrating injury
- biconvex with enhancement of the wall
- with area of necrosis

- In untreated, high mortality rates

o develops in association with osteomyelitis of the
skull, sinusitis, meningitis or penetrating trauma
o extraaxial fluid collections
o may extend to interhemispheric fissure or margin
of tentorium

Taenia solium
- Cysticercosis
- multiple small larvae are asymptomatic when alive
- encysted larvae dies eliciting inflammatory reaction leading
to seizures and ring enhancing brain lesions

- with calcified larvae in the brain parenchyma o

permanent na dyan

Meningitis
Infection in the subarachnoid space – leptomeninges
- secondary involvement of the epidura, dura, subdura, brain
parenchyma
- A medical diagnosis correlating with lumbar tap
- severe cases
Multiple Sclerosis
o pial and ependymal enhancement
Most common demyelenating disease
o abnormal signal or density of CSF because of
high protein content or frank pus - onset at age 20-50 years
- women > men
o brain edema
- manifest with clinical exacerbations and remissions
o stroke from vasospasm
 - with multiple plaques representing areas of demyelination
- with avid enhancement of sulcus and gyri highly
suggestive of meningitis
and varying inflammatory activity
MRI
- demonstrates plaques and follow up therapy response
- High dose steroid will prevent plaques from manifesting
- Involvement of the periventricular white mater, corpus
callosum
May involve the spine

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 MULTIPLE SCLEROSIS
 most common demyelinating disease
 onset at age 20-40 years  10% presenting in > 50 y/o
 women > men (2:1)
 manifest with clinical exacerbations and remissions
 multiple plaques representing areas of demyelination and varying
inflammatory activity
 tendency to involve periventricular white matter, corpus callosum and
visual system from the optic nerve to the occipital lobe; spinal cord
 MRI – used to demonstrate plaques; follow up of therapy response
 number and distribution areas do not correlate with clinical severity of
disease

 characterized by immune dysfunction with the production of abnormal

immunoglobulins and T cells, which are activated against myelin and
mediate the damage associated with the disease
 classic clinical definition of MS m
 multiple CNS lesions separated in both time and space.
 Patients may present with virtually any neurologic deficit, but
they most commonly present with limb weakness, paresthesia,
vertigo, and visual or urinary disturbances
 clinical course  characterized by unpredictable relapses and remissions
of symptoms
 diagnosis can be supported with clinical studies, which include visual,
somatosensory, or motor-evoked potentials and analysis of CSF for
oligoclonal banding, immunoglobulin G index, and presence of myelin
basic protein
 Histopathologically
 active MS lesions represent areas of selective destruction of
myelin sheaths and perivenular inflammation, with relative
sparing of the underlying axons.
 may occur throughout the white matter of the CNS, including
the spinal cord
 MR is the MOST SENSITIVE INDICATOR in the detection of MS plaques,
but imaging findings alone should never beconsidered diagnostic
 MS plaques will demonstrate contrast enhancement
 Enhancing lesions are indicative of acute lesions with active demyelination
and disruption of the blood–brain barrier

MULTIPLE MYELOMA
 Salt and pepper appearance
 diffuse and homogeneous low signal in the spine on T1WI, butmore
typically shows multiple focal defects
 Solitary plasmacytomas are in the differential diagnosis for vertebral
plana (totally collapsed vertebral body), along with eosinophilic
granuloma, leukemia, and severe osteoporosis.
 Technetium bone scans may miss myeloma lesions, which are often
relatively “indolent” metabolically.
 This has made MR spine “screening” of myeloma patents a useful practice

There’s no such thing as free lunch

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