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,
or nystagmus
 Physical signs : ecchymosis over the mastoid process (“Battle
sign”)
 Transverse Temporal Bone Fracture
o A liner or lucent area traversing the
petrous portion of the temporal bone
(perpendicular)
o Usually from a blow to occiput or frontal
region
o Complications: sensorineural hearing loss
 Longitudinal temporal Fracture
o Fracture is parallel to the petrous bone
o Sensorineural hearing loss uncommon
 Mix
 Prior to identifying fracture and where they are, you must have a
good anatomic picture of the brain
PRIMARY HEAD INJURY – EXTRA-AXIAL
EPIDURAL HEMATOMA
 Arterial in origin, result from skull fracture→ rupture that
disrupts the middle meningeal artery of the MCA
 Hematoma strips the dura → ovoid mass displaces adjacent
brain
 Skull fractures in 85-95%
 On CT/MRI→
 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!!
 occur between the dura and calvaria – constrained; resulting in
biconvex configuration

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

CEREBROVASCULAR DISEASE
 STROKE
 clinical term applied to any abrupt nontraumatic brain insult—
literally “a blow from an unseen hand.”
 caused by either brain infarction (75%) or hemorrhage (25%), and
must be distinguished from other conditions causing abrupt
neurologic deficits
 INFARCTION
 permanent injury that occurs when tissue perfusion is decreased
long enough to cause necrosis, typically due to occlusion of the
feeding artery
 TRANSIENT ISCHEMIC ATTACKS (TIAs)
 defined as transient neurologic symptoms or signs lasting less
than 24 hours, which may serve as a “warning sign” of an
infarction occurring in the next few weeks or months.
 are often due to temporary occlusion of a feeding artery
 HEMORRHAGE
 seen when blood ruptures through the arterial wall, spilling into
the surroundingparenchyma, subarachnoid space, or ventricles.
ISCHEMIC STROKE
- Secondary to thrombi or emboli
- CT Scan is the most commonly employed kase available
kung saan saan pero for ischemia it is MRI daw talaga
- Take a look at the hyperdense artery sign
o Arteries should not be seen in plain CT Scan but if
you see it then there must be an impending
infarct or ischemia within the distribution of that
artery
o Acute Trauma / Hemorrhage→ CT Scan!!
- White because of stasis of blood
- MRI is superior
o If you don’t see a flow void→ thrombus→
suspect infarct
o MRI show you the ischemic part in <6 hours
- Insular ribbon sign
o + swelling in the insula
CEREBRAL INFARCTION
 ischemic brain infarcts commonly due to atherosclerosis
 embolic brain infarcts result from emboli from the heart
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
 subtle obliteration of the cortical sulci
 reduced density related to vascular distribution
 poorly defined, heterogeneous reduced density; may or may
not cause mass effect
 may have sharp margin and homogeneous attenuation
 MRI findings
 demonstrates ischemic changes earlier than CT
 on T1-weighted images - decreased signal intensity with loss of
normal signal difference between gray and white matter
 on T2-weighted images - increased signal intensity
 small hemorrhages in the infarcts are seen on MRI but not seen
on CT
HYPERTENSIVE HEMORRHAGES
 often occur in the
 external capsule
 thalamus
 internal capsule
 cerebellum
 pons
 lobar white matter
seen in the putamen (35% to 50%)
subcortical white matter (30%),
cerebellum (15%),
thalamus (10% to 15%), and
pons (5% to 10%)
 frequently rupture into the ventricular system
 areas of high density with sharply defined borders
 no edema in acute bleed; edema develops after several days
 Small hypertensive hemorrhage may resolve with few deficits.
 poor prognosis
 Bleeds in the posterior fossa, those with a large amount of mass
effect
 hemorrhages extending into the ventricular system
 Focal contrast extravasation within an acute hematoma on CTA or
routine contrast-enhanced CT images (“spotsign”) predicts a high risk
of clot expansion over the first several hours after admission compared
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
o edge of sphenoidal ridge
o margin of falx cerebri and tentorium
- derive blood supply from arteries supplying the dura
o may parasitize vasculature of adjacent brain
o may obstruct dural sinuses
o most incite osseous response (ie. hyperostosis)
and may invade bone producing hyperostotic
density on outer table
o may produce bone destruction
o some completely destroys bone, with a soft-tissue
mass bulging externally
o calcification found in 15-20%
o small punctate densities
o sand-like deposits = psammoma bodies
o some form densely calcified masses
o homogeneous enhancement on contrast
administration, with well defined margin and with
an adjacent dura tail
- MR shows hypointense lesion (T1W) and hyperintense
(T2W), with sharply defined magins
Dural
Tail
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Intraventricular Tumors
- Lobulated, whitish structures
o Must be differentiated from haemorrhage, the
difference is that haemorrhage is no lobulated
saka pag haemorrhage dapat nag po pool sa
dependent portion
Pituitary Adenoma
Classified as hormonally active versus hormonally inactive
- hormonally active adenomas are further subdivided
according to the hormone they secrete
- depending on size , classified as
o macroadenoma (>1cm)
o microadenoma (<1cm)
- macroadenomas, usually hormonally inactive, become
clinically manifest as a result of their size, compressing
adjacent neural structures (ie. optic chiasm)
- microadenomas seek medical attention because of
abnormal hormone secretion
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
- ACTH-secreting adenomas - Cushing’s disease
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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