CNS RADIOLOGY 1st sem SY 2014

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NERVOUS SYSTEM

Looking at the brain:
 Midline
 Symmetry
 Basal Cisterns
o Quadrigeminal Plate
o Suprasellar
 Ventricles
o Suprasellar
o Pineal
o Craniocervical region

EXAMINATION OF THE CENTRAL NERVOUS SYSTEM
 skull radiograph
 ultrasound
Cranial Ultrasound:
CSF black
Hemorrhage white
 computed tomography (CT)
Cranial CT Scan
Brain window brain is being assesed
Bone window bone is being assesed
Punched-out lesion metastasis or
meningioma
 angiography
 radionuclide (nuclear imaging)
 magnetic resonance (MR) for soft tissue imaging
MR Spectroscopy (MRS)
o Newer modality
o Each peak of metabolites has corresponding
pathologic diagnosis
o Available in 1.5 – 3.0 TESLA machine
o Metabolites
 Choline  tumor
 N-acetyl aspartate (NAA)
 Creatine
 Lactic Acid  inflammation
Diffusion-Weighted MR Imaging
o Used by neurologists to diagnose ischemic strokes
o <6 hours of infarct/ischemia is diagnostic on
DWI/ADC-time restricted diffusion
o FMRI (functional MR imaging)
CT SCAN IS THE TECHNIQUE OF CHOICE FOR:
 evaluation after acute trauma
 suspected acute intracranial hemorrhage
 diseases of the skull base or calvaria
 when MRI is contraindicated
REASONS FOR THE USE OF INTRAVENOUS CONTRAST
MEDIUM
 iodinated contrast (for CT) and gadolinium paramagnetic
contrast (for MR) do not cross the blood brain barrier
 in the presence of pathology/ disruption of the BBB,
contrast will localize in the site of pathology
 also improves definition of vascular and dural structures

X-RAY AND 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

ANGIOGRAPHY AND RADIONUCLIDE IMAGING
 many of the indications for cerebral angiography have been
eliminated by CTA, MR and MRA
 radionuclide imaging has specific roles in seizure disorders,
dementia, psychiatric disorders, brain death

MRA
Analysis of the abnormality
o Intraaxial in the parenchyma
o Slightly, moderate, or markedly enhanced?
o Cystic or fluid?
o Solid or heterogenous?


INTRACRANIAL CALCIFICATION AND OSSIFICATIONS

Physiologic Intracranial Calcifications
 pineal gland
 habenular commissure
 choroid plexus
 dura
 Pacchionian bodies
 basal ganglia and dentate nucleus

PINEAL GLAND CALCIFICATION
 almost always present in the adult
 Rare before 6 years old
 cluster of amorphous irregular calcifications, or may be
solitary
 usually 10-12 mm in greatest diameter; usually 3-5 mm
 calcifications greater than 1 cm, suspect pineocytoma or
AVM
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CHOROID PLEXUS CALCIFICATION
 almost all adults; also frequent in children
 frequently seen at the glomera (atria of lateral ventricles)
DURAL CALCIFICATIONS
 plaque-like calcification
 common in the falx and in the edges of the tentorium
 free edges of the tentorium posterior to the sella (the
petroclinoid ligaments) are prone to dense calcifications
 may be part of the basal cell nevus syndrome

CEREBROVASCULAR DISEASES
 Ischemic Stroke
 Etiology
 CT Scan
 Hypodense artery sign
 MRI is superior
 Normal black signal

EDEMA
 increase in fluid in the brain tissue
 primarily intracellular because of some insult to the cell =
cytotoxic edema
 may be extracellular related to loss of blood-brain barrier =
vasogenic edema

CYTOTOXIC EDEMA
 seen in strokes, hypoxemic injury (near-drowning), viral
cerebritis, cortical edema from status epilepticus
 seen in neuronal cell bodies ( in gray matter)
 on CT, leads to diminished density of gray matter
 blurring or loss of distinction between gray and white
matter
 on MRI, diminished signal on T1-weighted images, and
increased signal on T2-weighted images

VASOGENIC EDEMA
 seen in metastatic or primary neoplasm, infections
 primarily a white matter phenomenon because the
intercellular spaces are larger in the white matter, with
notable exception of the corpus callosum

EDEMA
 increased brain volume versus fixed volumes of the
intracranial compartments
 may cause brain tissue to be deformed or to herniate from
one compartment to another

EDEMA INJURY
 may lead to death with downward brainstem herniation or
cerebellar tonsillar herniation, which compromise the
medulla
 death through an overall pressure effect
 death from ischemia when intracranial approaches or
exceeds arterial perfusion pressure
 direct physical deformation of the brain parenchyma
 injury of the brain along the edges of the dural reflections
across which it is squeezed
 pressure on other portions of the brain
 compromise of the vascular supply
 compromise of other structures (ie. cranial nerves)

ACUTE MCA ISCHEMIA ON CT
 Insular ribbon sign
 Lentiform nucleus edema sign

CT SCAN AND MRI IN ISCHEMIA
Left temporoparietal lobe  thrombus

CNS NEOPLASMS
Approach to radiographic abnormality
 Is it a mass?
 Intraaxial or extraaxial?
 Tumor margins
 MRI is modality of choice for intracranial neoplasm

NEOPLASMS: GENERALITIES
 classified by anatomic location and cell of origin
o intraaxial = lesion within the brain
o extraaxial = lesion outside the brain
 70% of tumors in adults are supratentorial
 most tumors in children are infratentorial
 most common primary tumors in adults - astrocytomas,
glioblastomas
 most common primary tumor in children - astrocytoma of
the cerebellum or brainstem
 extraaxial location of tumor = more favorable prognosis

NEOPLASMS: INCIDENCE
 gliomas = 43%
 meningiomas = 15%
 pituitary adenomas = 13%
 acoustic neuromas = 6.5%
 congenital tumors = 4%
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 blood vessel tumors = 3%
 miscellaneous = 9%

INTRACRANIAL TUMORS

GLIOMAS
 graded from 1 to 4, grade 4 being most malignant
 grade 1 and 2 are the more benign astrocytomas
 grade 3 are anaplastic astrocytomas
 grade 4 are glioblastoma multiforme
 classification may include cell morphology (fibrillary or
pilocytic), and site of origin (supra- or infratentorial)
 gliomas seldom of pure histologic type

GLIOBLASTOMA MULTIFORME
 invasive, malignant tumor of astrocytic origin
 most common supratentorial glioma
 Butterfly glioma
 between 40-60 years
 rapid onset of symptoms; infiltrative; spread rapidly
 involvement of both cerebral hemispheres via spread
through corpus callosum common
 may spread through ventricular system or subarachnoid
space
 true multicentric tumors are rare
 MR - increased signal intensity is related to vasogenic
edema
 show marked enhancement on contrast
 enhancement because of tumor neovascularity and the
resulting increased permeability of the BBB
 margins of the tumor are irregular
 pattern of contrast enhancement is heterogenous
 mass effect is usually present
 if the frontal or parietal lobes are involved, usually crosses
midline and deformity of both ventricles occur
 central necrosis of the tumor occurs
 cysts sometimes occur
 difficult to accurately differentiate the infiltrating margin of
the tumor form adjacent normal brain tissue
 CT demonstrates less of the pathologic findings than MR
o Ring enhancing lesions (MAGIC DR)
o Contralateral heterogenous enhancing margins

ANAPLASTIC ASTROCYTOMA
 second most common supratentorial glioma
 less infiltrative and less rapid than glioblastoma multiforme
 comprise 32% of all supratentorial tumors

LOW-GRADE ASTROCYTOMA
 symptoms duration to the time of diagnosis usually 3 years
 large cysts usually form in astrocytomas
 cystic element may predominate in the pathologic and
radiographic appearance
 calcification occurs in the minority
 variable degree of enhancement on contrast
 for small lesions, CT may be normal or show only mass
effect, with displacement, distortion or compression of the
ventricles
 MR is more accurate than CT in demonstrating the borders
of the lesion

JUVENILE PILOCYTIC ASTROCYTOMA
 variety of low-grade astrocytoma that occurs in children
 occurs in or adjacent to the visual pathways or posterior
fossa
 well-defined; enhance markedly on CT and MR
 cyst formation is common

OLIGODENDROGLIOMA
 7% of supratentorial gliomas
 average age at time of diagnosis is 45 years
 grow slowly, duration of symptom to diagnosis is 11 years
 occurs almost exclusively in the cerebral
hemispheres
 predilection for frontal lobes
 calcification (course, irregular strands within the tumor
occurs frequently) on CT Scan
 lack of neovascularity and minimal disruption of BBB,
contrast enhancement is slight
 cystic and necrotic changes are rare

INTRAAXIAL TUMORS: NON-GLIAL AND MIXED GLIAL

PRIMARY CNS LYMPHOMA

EPENDYMOMA
 5% of supratentorial gliomas
 duration of symptom to diagnosis is short, usually 1 year
 average age at diagnosis is 30 years
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 infratentorial ependymomas occur in children and
adolescents; more common than the supratentorial form
 arise from ependymal cell nests at margin of lateral
ventricles
 occur near the atrium of the lateral ventricles
 often contain scattered small or punctate calcium deposits
 cystic changes may occur
 enhances on contrast

MENINGIOMA
 extraaxial tumors that arise from the arachnoid
 majority are benign
 common sites
• along superior sagittal sinus
• region of tuberculum sellae or anterior to the
tuberculum along the olfactory groove
• edge of sphenoidal ridge
• margin of falx cerebri and tentorium
 derive blood supply from arteries supplying the dura
 may parasitize vasculature of adjacent brain
 may obstruct dural sinuses
 most incite osseous response (ie. hyperostosis) and may
invade bone producing hyperostotic density on outer table
 may produce bone destruction
 some completely destroys bone, with a soft-tissue mass
bulging externally
 calcification found in 15-20%
 small punctate densities
 sand-like deposits = psammoma bodies
 some form densely calcified masses
 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

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 ACTH-secreting adenomas - Cushing’s disease

PITUITARY MICROADENOMA
 contrast MR - reduced signal intensity (on T1W) on top of
an enhancing pituitary gland
 increased height of the gland (usually <10mm) with
alteration in contour of the upper margin of the gland
 erosion of the floor of the sella turcica
 displacement of the normally midline pituitary stalk

PITUITARY MACROADENOMA
 contrast MR - marked homogeneous enhancement
 cystic or necrotic areas in large macroadenomas

CRANIOPHARYNGIOMA
 congenital tumor which arises from remnants of Rathke’s
Pouch
 tumor of childhood and adolescence
 In young children, clinical complaints are related to
increased intracranial pressure
 In older children and adults, symptoms are visual or
endocrine in nature (ie. Delayed growth)
 calcification occurs in 80%
 most are suprasellar; 10-15% within the pituitary fossa
 cystic changes may occur
 variable appearance on MR depending on the amount of
calcification (low intensity on T1w and T2W) and cystic
change (high signal on T1W and T2W)
 solid portions of the tumor enhance in a homogeneous
manner

SCHWANNOMA
 benign tumors occuring along the course of cranial, spinal
and peripheral nerves
 previously called neuromas or neurilemmomas which are
misleading
 adults; 2W:1M
 eighth cranial nerve most frequently involved; fifth nerve
also
 of the VIII CN - hearing loss, tinnitus, vertigo or dizziness
 most common tumor of the cerebellopontine angle
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 CT - large lesions will obliterate the CP angle, displace
brainstem and IV ventricle, and widen the contralateral CP
angle cistern
 small lesions may only enlarge the internal auditory canal
 enhances considerably on contrast
 MR - reduced signal on T2W; intense enhancement on
contrast
Acoustic Schwannoma  CT angle : pontine involvement

METASTASIS TO THE CNS FROM EXTRACRANIAL SITES
o Intraaxial
o Extraaxial
o Hemorrhagic
o On CT and MRI
o Intense enhancement

Leptomeningeal Carcinomatosis

METASTASIS
 most arise from hematogenous spread
 tends to occur in the distribution of the end-arteries, hence
at the gray-white matter junction, and in the distribution of
the deep perforating arteries
 melanoma, lung, breast, colon, kidneys
 CT and MR findings vary, depending on the primary source
(ie. cellularity), vascularity and biological behavior, number
and location of tumors, and previous treatment
 CT - often multiple, fairly discrete, surrounded by low
density edema
 calcification is unusual (except osteogenic sarcoma)
 tendency to hemorrhage spontaneously (melanoma, renal
cell, choriocarcinoma)
 contrast CT - most will enhance, though variable in pattern
 MR - hypointense on T1W, heterogenously hyperintense on
T2W
 most enhance on contrast administration

POSTERIOR FOSSA TUMORS
Choroid Plexus Papilloma
Carcinoma
Colloid Cyst

HEAD TRAUMA
 MRI is not needed in Acute Head Trauma
 Skull Xray is not helpful
 Assess whether scalp injury or skull injury
 CT is the diagnostic method of choice; MRI slowly
supplanting CT
 detection of hemorrhages - subarachnoid,
intraparenchymal, extraaxial (subdural, epidural)
 contusions, diffuse axonal (shearing) injury, diffuse brain
swelling

HEAD TRAUMA: PARENCHYMAL HEMATOMA
 increased density on CT
 margins are irregular but very distinct
 homogeneous in character
 occur most frequently in the inferior frontal and temporal
lobes, and basal ganglia
 extraventricular obstructive hydrocephalus – arachnoid
scarring lead to blockage of CSF absorption

SUBARACHNOID HEMORRHAGE


HEAD TRAUMA: BRAIN CONTUSION
 may not be visualized on CT initially, unless large or
associated with hemorrhage
 become apparent 1-2 hours after injury
 mixed high and low density - small hemorrhages with
surrounding edema
 frontal and temporal lobes adjacent to calvaria
CORTICAL CONTUSIONS
 in the brain cortex
 Areas
 Multiple
 Common sites
 On CT
 Salt and pepper pattern
 On MRI

SUBDURAL HEMATOMA
 bleeding into subdural space
 over the convexity of the cerebral hemisphere
 early detection by CT has reduced mortality in acute
subdural hematomas
 appearance varies on
o age of blood
o whether repeated episodes of bleeding occurred
o unilateral or bilateral
o level of patient’s hematocrit (has haematocrit
effect)
 hyperdense, isodense, hypodense
o hyperdense in early stage - 1 to 10 days
o isodense - 1 to 3 weeks
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o hypodense - after 1 month
 crescentic configuration crescent shape bleeding
 mass effect is greater than the size of the hematoma;
reflect underlying brain swelling and injury that accompanies
the hematoma
 in large hematomas, medial margin may be straight or
convex, simulating epidural
 hematoma may be heterogeneous even in acute bleed if
there is incomplete clotting due to disorder of clotting
mechanism
 chronic subdural hematoma

EPIDURAL HEMATOMA
 result of injury to meningeal vessels (arterial)
 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)
 occur between the dura and calvaria – constrained resulting
in biconvex configuration
 may cross the midline because they are external to the falx
 do not cross sutures

INTRAVENTRICULAR HEMORRHAGE
 may puti

DIFFUSE AXONAL INJURY
 m

INTRACEREBRAL HEMORRHAGE
Subcortical gray matter injury
Multiple petechial hemorrhage

CNS INFECTION
 pyogenic
 atypical bacterial
 fungal
 viral
 parasitic
 prion (slow virus)

Viral Meningoencephalitis
 diagnostic neuroimaging is optimized by clinical
information
 neuroimaging patterns are limited

MENINGITIS
 infection in the subarachnoid space - leptomeninges
 secondary involvement of the epidura, dura, subdura,
brain parenchyma
 severe cases
o pial and ependymal enhancement
o abnormal signal or density of CSF because of high
protein content or frank pus
o brain edema
o stroke from vasospasm

SUBDURAL AND EPIDURAL EMPYEMA
 in untreated, high mortality rates
 develops in association with osteomyelitis of the skull,
sinusitis, meningitis or penetrating trauma
 extraaxial fluid collections
 may extend to interhemispheric fissure or margin of
tentorium

CEREBRITIS AND BRAIN ABSCESS
 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
 CT - areas of hypodensities, with little enhancement on
contrast
 later, neovascularity and collagen capsule develop; ring
enhancement become apparent

ATYPICAL BACTERIA, FUNGI AND PARASITES
 taenia solium
o cysticercosis
o multiple small larvae are asymptomatic when alive
o encysted larvae dies eliciting inflammatory
reaction leading to seizures and ring enhancing brain
lesions

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CEREBRAL INFARCTION
 ischemic brain infarcts commonly due to atherosclerosis
 embolic brain infarcts result from emboli from the heart
 other causes - primary arterial diseases such as
fibromuscular hyperplasia, arterial dissections and arteritis;
venous occlusive disease; septic or tumor emboli
 CT most commonly employed
 MRI is superior
 CT scan findings depend on
o size of the abnormality
o association with significant hemorhage
o time interval between the time of infarct and the
time of CT scan
o 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
o loss of distinction with the gray and white matter
o subtle obliteration of the cortical sulci
o reduced density related to vascular distribution
o poorly defined, heterogeneous reduced density;
may or may not cause mass effect
o may have sharp margin and homogeneous
attenuation
 MRI findings
o demonstrates ischemic changes earlier than CT
o on T1-weighted images - decreased signal intensity
with loss of normal signal difference between gray
and white matter
o on T2-weighted images - increased signal intensity
o small hemorrhages in the infarcts are seen on MRI
but not seen on CT

BRAIN INFARCTION
 Loss of
 Subtle
 Reduced density
 Infarction black on CT Scan

VASCULAR INJURIES
 Arterial
 Internal carotid injury
 Carotid cavernous fistula
o On MRI
o Proptosis
o Selective carotid angiography with rapid
flowing
 Cavernous sinus in middle portion
 Inferior Carotid Artery

Hemorrhagic Transformation of Infarction
 Peak time is 1-10weeks, 2 weeks most infarction
happen
 Petechial gyral pattern
 Large cortical infarcts

Watershed (Borderzone) Infarction
 Infectious
 Rosary head sing

SMALL VESSEL ISCHEMIA
 Lacunes “little lakes” as a result of
 Differentiated from Virchow robin spaces which is
benign

Venous Infarction
 Venous clot scar

Empty delta sign
 Pattern of hemorrhagic infarction

Parenchymal Hemorrhage

Vascular Malformations
Primary hemorrhage VS hemorrhagic neoplasms
Primary hemorhhage VS hemorrhagic transformation of
infarction (infarct that becomes hemorrhagic again)

HYPERTENSIVE HEMORRHAGES  200/100mmHg
 often occur in the
o external capsule
o thalamus
o internal capsule
o cerebellum
o pons
o lobar white matter
 frequently rupture into the ventricular system
 areas of high density with sharply defined borders
no edema in acute bleed; edema develops after several days

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INTRACRANIAL ANEURYSM
 dilatation of an artery
 saccular/berry aneurysm - result of hemodynamic stresses
 other types - atherosclerotic, mycotic (infectious),
posttraumatic
 become symptomatic because of rupture leading to
subarachnoid and intraparenchymal hemorrhage

SACCULAR ANEURYSMS  berry aneurysm
 very common, up to 5-9% of the adult population
 most aneurysms never rupture
 once rupture occurs, 60% will either die or develop
neurologic dysfunction
 occur at points of major arterial branching
 most common sites
o proximal segment of middle cerebral artery
o anterior communicating artery
o junction between the internal carotid and
posterior cerebral artery
 size from less than 1 mm to more than 5 cm
 those > 2.5 cm = giant aneurysm

INTRACRANIAL ANEURYSMS
 suspected subarachnoid hemorrhage - do NECT (non
enhanced CT)
 unilateral location, above or below the tentorium gives
evidence as to where the lesion is most likely located

SECONDARY HEAD INJURIES
 Diffuse Cerebral Swelling
 Brain Herniation
 Hydrocephalus
 I?
 CSF Leak
 Leptomeningeal cyst
 Encephalomalacia

Diffuse Cerebral Swelling

Brain Herniation
 Subfalcine (cingulate) herniation
 Uncal herniation medal temporal lobe downward
 Transtentorial herniation upward or downward
 External outward through skull defect
 Tonsillar herniation downwad to craniocervical
junction

Hydrocephalus

I?

CSF Leak
Dural Tear
Calvaria
CSF rhinorrhea
CSF otorrhea

Leptomeningeal cyst
Growing fracture
Traumatic tear in the dura

Encephalomalacia
Focal

Penetrating Wound
Gunshot wound

Child Abuse
 Skull fracture
 Subdural hematoma
 Whiplash shaken injury
 Chronic subdural hematoma
 Diffuse brain swelling

MULTIPLE SCLEROSIS
 most common demyelinating disease
 onset at age 20-50 years
 women > men
 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

MULTIPLE MYELOMA
 Salt and pepper appearance

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PARANASAL SINUSES
 Frontal, maxillary, sphenoid, ethmoids
 AP, Water’s view and Lateral view ON X-RAY
 CT SCAN and MRI

CROUP (Laryngotracheobronchitis)
 AP view of the neck
 NORMAL versus ABNORMAL (steeple sign)

Source:
-Old trans
-Brant and Helms Diagnostic Radiology 4
th
Edition