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DIAGNOSTIC IMAGING METHODS IN CENTRAL cyst

NERVOUS SYSTEM DISORDERS Colloid cysts
P. Danilo J. Lagamayo, MD Anterior pituitary gland Pituitary adenoma
Adenocarcinoma
(Radiology/ Lecture Date: July 6, 2006) Local extension Chordo from adjacent
Glomus jugulare
tumors
HEADACHE:
Chondroma
• Primary: Chondrosarcoma
- Migraine Cylindroma
- Cluster
- Tension
Incidence of Tumors:
• Secondary: Glioblastoma - - - - - - - - - 55%
- Increased Intracranial Pressure: Astrocytoma - - - - - - - - - 20.5%
o Neoplasms Ependymoma - - - - - - - - 6%
o Abscess Medulloblastoma - - - - - - 6%
o Granulomas Oligodendroglioma _ - - - 5%
- Meningeal Irritations: Choroid Plexus Papilloma 2%
o Meningitis
Other less common entities:
o Subarachnoid Hemorrhage Neuronal tumors – Gangliocytomas,
- Vascular Disorders: Ganglioglioma
o Stroke Embryonal – NET
o Malformations Pineal Region – germ cell
o Arteritis Primary CNS Lymphoma
- Head Trauma:
o Concussion
o Hematoma Primary Imaging Methods for Diagnosis of CNS
tumors
- Other Cranio-Facial Pains:
MRI
o Trigeminal Neuralgia
CT SCAN
ANGIOGRAPHY
Incidence of Primary Brain Tumors:
- 6 persons / 100,000 population / year CT SCAN
- about 1 in 12 primary brain tumors occur in • Advantages
children under 15 years old. - Wide availability;
- Can accommodate life support systems;
Clinical Presentation of Brain Tumors: - Fast imaging methods
- Focal neurologic deficit - Can show bone structures and their pathologic
- Increase intracranial pressure: changes like fractures;
o Headache that is more severe in AM - Cheap.
o Nausea / Vomiting • Disadvantages
o Diplopia - Cannot demonstrate soft tissue detail of the sella
o Papilledema turcica, the brain stem and the cerebellum;
o Ontundation & Lethargy (ominous) - Not very sensitive to white matter lesions;
- Cannot differentiate encephalomacic lesions of
- Focal neurologic signs and symptoms: hemorrhage from infarcts;
o seizure, seen in about ½ of patients - Uses ionizing radiation and cannot be used on
- Non-localizing findings: pregnant patients.
o Fatigue
o malaise MRI
o impotence • Advantages
o galactorrhea - Unaffected by the thick bone encasement of the
o growth failure calvarium in the posterior fossa and the sellar
turcica;
o macrocephaly in young children
- Accurate determination of the age and evidence
of hemorrhage;
Pathological Classification of Intracranial Tumors: - More sensitive for detection of white matter
lesion;
Neuro- Astrocytes Astrocytoma - Ability to perform multiplanar imaging;
epithelial Oligodendrocytes Oligodendroglioma - Does not use radiation and can be safely used on
Ependymal cells & Ependymoma pregnant patients.
Choroid Plexus Choroid Plexus • Disadvantages
Papilloma - Longer time needed to complete an examination;
Neurons Gangliomas, - Needs patient cooperation, e.g. patient must not
Gangliocytomas, move during an imaging sequence that can take
Neuroblastomas anywhere from 1 minute to as long as 7 minute;
Pineal cells Pineocytomas - Any metal implement is not allowed into the MR
Pineoblastomas room.
Poorly Glioblastoma - Cannot image patients with:
differentiated and multiforme o Pacemakers
embryonic cells Medulloblastoma o Neurostimulators
Meninges Meningioma o Newly applied vascular clips
Nerve sheet cells Neuroma o Vacular clips with ferromagnetic
Neurofibroma materials (steel or iron)
Blood vessels Hemangioblastoma o Metal foreign bodies in the orbit
Germ cells Germinoma Teratoma o Claustrophobic patients
Tumors of maldevelopmental Craniopharyngioma o Patients who need extensive life support
origin Epidermoid/Dermoid
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- Iron with dystrophic Ca or necrosis

Causes of LOW Signal Intensity in Tumors in T2WI: - Ferritin/hemosiderin from prior bleed
• Paramagnetic effects - Deoxy hgb in acute bleed
- Intracellular met hgb in early subacute bleed
- Melanin (or other free radicals)
• Low spin density
- Calcifications
- Scant cytoplasm (high nucleus:cytoplasm ratio)
- Dense Cellularity Magnetic Resonance Criteria for Cystic Lesions
• Fibrocollagenous stroma
• Macromolecule content Morphology Sharply demarcated, round smooth
• Very high (non-paramagnetic) protein content Signal Intensity Isointense to cerebrospinal fluid on all
• Intratumoral vessels spin echo images (tumor cysts can be
- Signal void from rapid flow hyperintense due to ↓ T1)
Fluid-debris Intracellular blood-cyst fluid
Causes of High Signal Intensity in Tumors in T1WI: levels Intracellular blood-extracellular blood
• Paramagnetic effects from hemorrhage (bleed into
- Subacute – chronic blood (met hgb) necrotic or
• Paramagnetic materials w/out hemorrhage cystic regions)
- Melanin Motion of intra- Lesion emanates ghost images along
- Naturally occuring ions associated with necrosis lesional fluid phase-encoding axis
of calcification: Manganese, Iron, Copper Intralesional signal loss (especially on
• Non-paramagnetic effects steady-state sequences)
- Very high (non-paramagnetic) proteins
- Fat Hemorrhagic Tumors
- Flow related enhancement in tumor vessels Primary brain tumors
Glioblastoma/anaplastic asctrocytoma
Requirements for contrast enhancement: Anaplastic
- absence of blood-brain barrier oligodendroglioma/oligodendroglioma
- adequate delivery of contrast material Ependymoma
Teratoma
- extracapillary interstitial space to accommodate Metastatic disease
contrast
Melanoma
- appropriate contrast dosage
Renal cell carcinoma
- spatial resolution
Choriocarcinoma
- imaging parameters to allow contrast detection Lung carcinoma
- time for contrast to accumulate in the region of Breast carcinoma
interest Thyroid carcinoma

Mechanism for contrast enhancement in CNS tumors: Intratumoral Hemorrhage vs. Benign Intracranial
- Formation of capillaries with deficient blood-brain Hematomas
barrier rather than the destruction of blood-barrier
is presumed as the mechanism for tumor • Intratumoral hemorrhage:
enhancement. - Markedly heterogenous, related to:
- The capillaries of metastatic tumors to the brain o Mixed stages of blood
has no blood-brain barrier since these tumors o Debris-fluid (intracellular-extracellular
come from elsewhere and not from the brain. blood) levels
o Edema + tumor + necrosis with blood
Type of enhancement: - Identification of nonhemorrhagic tumor
- immediate or delayed component
- evanescent or persistent - Delayed evolution of blood breakdown products
- dense and homogenous - Absent, diminished, or irregular
- minimal or irregular ferritin/hemosiderin
- Persistent surrounding high intensity on long TR
Note: Lack of tumor enhancement do not signify images (i.e., tumor/edema) and mass effect,
lack of tumor. even in late stages
• Benign hemorrhage:
Effects of Tumor Necrosis on Signal Intensity: - Shows expected signal intensities of acute,
subacute or chronic blood, depending on stage of
Short relaxation Hemorrhage hematoma
times Liberation of cellular iron - No abnormal nonhemorrhagic mass
Release of free radicals - Follows expected orderly progression
Proteinaceous debris - Regular complete ferritin/hemosiderin rim
Prolong Cystic change with - Complete resolution of edema and mass effect in
relaxation times increased water chronic stages

Frequently Cystic Tumors

Colloid cyst
Craniopharyngioma
Desmoplastic infantile ganglioma
Dermoid
Ependymoma (supratentorial and spinal)
Epidermoid
Ganglion cell tumors
Glioblastoma (cystic necrosis)
Hemangioblastoma
Pilocytic astrocytoma
Pleomorphic xanthoastrocytoma
Rathke cleft cyst
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CLASSIFICATION OF ASTROCYCTIC BRAIN TUMORS

Diffuse (infiltrative) Localized (circumscribed)

Astrocytoma
Anaplastic astrocytoma
Glioblastoma multiforme
Pilocytic astrocytoma
Pleomorphic
xanthoastrocytoma
Subependymal giant cell
astrocytoma

DIFFUSE ASTROCYTIC BRAIN NEOPLASMS

Astrocytoma Anaplastic Glioblastoma Gliomatosis
astrocytoma
Typical site(s) of Cerebral Cerebral Cerebral Cerebral
origin hemisphere (adult) hemisphere (adult) hemisphere hemisphere (young
Brainstem (child) Brainstem (child) (adult) or middle-aged
Cerebellum (young adult)
adult)

Signal intensity Homogeneous; Some Markedly Ill-defined; high

characteristics highintensity heterogeneity heterogeneous; intensity
(on T2-weighted hemorrhage and
image) necrosis common

Vascular flow voids Not seen Unusual Common Rare

Contrast
enhancement Variable; irregular Common; irregular Common; irregular Uncommon

Prognosis (median 7-8 yr 2-3 yr 12 mo Estimated as

survival, if months
available)

PEDIATRIC SUPRATENTORIAL HEMISPHERIC NEOPLASMS

Juvenile Ganglioglioma Pleomorphic Embryonal DNT
pilocytic xanthoastrocytoma tumor
astrocytoma (e.g., cerebral
neuroblastoma)
Signal intensity Sharply Sharply Sharply Markedly Sharply
characteristics demarcated; demarcated; demarcated heterogeneous demarcated
(on T2- commonly cystic commonly cystic with subjacent cyst heterogeneous
weighted
image)

Contrast Common; dense Common; irregular Common in solid Common; Unknown

enhancement portion irregular

Hemorrhage Rare Rare Rare Common Rare

Calcification Uncommon Common Uncommon Common Common

Prognosis Excellent Excellent Variable Poor Excellent

INTRAVENTRICULAR MASSES
Tumor type Typical location Intensity characteristics on T2- Contrast enhancement
weighted images **
Central neurocytoma Lateral Isointense to gray matter Usually dense
(attached to septum
pellucidum)

Ependymoma Fourth, lateral Heterogeneous Heterogeneous

Subependymoma Lateral, fourth Hyperintense to gray matter None

Oligodendroglioma Lateral Heterogeneous Variable; irregular

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Pilocytic astrocytoma Lateral, third, or fourth Hyperintense to gray matter Dense

Meningioma Lateral (atrium) Isointense to gray matter Dense

rd
Choroid plexus tumor Lateral (atrium) or 3 in Heterogeneous None
children, 4th in adults

Epidermoid Any ventricle Slightly hyperintense to CSF Generally enhance

Subependymal giant Lateral Hyperintense to gray matter Limited enhancement at periphery

cell astrocytoma

Colloid cyst Third Hyperintense to gray matter None

Arachnoid cyst Any ventricle Isointense to CSF

Important Note: the column “Intensity Characteristics on T2 Weighted images” lacked 1 lineand very much misaligned in the powerpoint file
given to us. Pls verify with references.
POSTERIOR FOSSA TUMORS IN CHILDHOOD
Juvenile pilocytic Medulloblastoma Ependymoma Diffuse pontine
astrocytoma glioma
Signal intensity Sharply Homogeneous; Markedly Ill-defined; high
Characteristics demarcated; low to moderate heterogeneous intensity
(on T2-WI) commonly cystic intensity

Contrast enhancement Common in Common; dense Common; irregular Variable

solidportion (mural
nodule)

Calcification Uncommon Uncommon Common Rare

Hemorrhage Rare Uncommon Common Common

Tendency to seed Extremely low High Low to moderate Low

CSF pathways

Prognosis >90% 10-yr 50% 5-yr survival 65-70% 5-yr <1-2% 5-yr survival
(estimated survival) survival survival

PINEAL REGION TUMORS

Germinoma Teratoma Pineoblastoma Pineocytoma Glioma Meningioma
Age; sex Child; male Child; male Child; none Adult; none Child; none Adult; none
predilection

Pineal vs. Pineal Pineal Pineal Pineal Parapineal Parapineal

parapineal (usually) (usually)

Signal intensity Homogeneous Strikingly Homogeneous Variable Homogeneou Homogeneous

(heterogeneous (but often heterogeneous (unless s
vs.homogeneous) hemorrhagic) hemorrhagic) (usually)

Hemorrhage Common Typical Common Common Rare

Rare
Calcification Rare Typical Common Common Common
Common
Brain edema or Common Variable Common Uncommon Occasional
invasion Primarily
midbrain
Tendency to Yes Variable Yes No No
metastasize Variable

Enchancement Dense Variable Dense Dense Dense

Variable
Prognosis Excellent Variable Poor Variable Excellent
Variable

MAGNETIC RESONANCE FINDINGS IN EXTRAAXIAL MASS LESIONS

Suggestive Definitive
Peripheral, broadly based along calvarium Cerebrospinal fluid cleft between brain and lesion

Overlying bone changes Vessels interposed between brain and lesion

Enhancement of adjacent meninges Cortex between mass and (edematous) white matter

Displacement of brain from skull Dura (meninges) between (epidural) mass and brain

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STROKE
- a new, often acute, loss of neurologic function
secondary to parenchymal ischemia or
hemorrhage.
Main Etiologies for Symptomatology of Stroke:
1. Cerebral Infarction
2. Intraparenchymal Hemorrhage
3. Subarachnoid Hemorrhage
Role of Imaging in Stroke:
1. Rule out hemorrhage
2. Rule other causes of stroke
3. Help assess etiology in known ischemic infarction
The Normal Brain:
• To sustain the normal brain, a normal mean
regional cerebral blood flow (rCBF) must be
maintained at about 54 (± 12 ml) / 100 g / min
• The threshold for cerebral ischemia is
approximately at: 23 ml / 100 g /min.
• Autoregulation plays a very important role in
maintaining intracerebral blood flow. This
mechanism can be temporarily lost in ischemia
leaving the control of blood flow to peripheral flow
volumes.
Ischemic Strokes:
• Large Artery or Atherosclerotic Infarction
• Cardioembolic Infarction
• Small Vessel Infarction
• Venous Infarction
The Abnormal Brain:
• Between cerebral blood flow rate of
15 & 20 ml / 100 gm / min.,
ischemic brain injury begins w/ loss of neurologic
function, noted as flattening of the
electroencephalogram.
This may still be reversible.
• Blood flow values below:
10 ml / 100 gm / min.,
may lead to infarction within a few minutes.
The Ischemic Brain:
• There are two ischemic changes thresholds:
o one occurring at blood flow range of
15-20 ml / 100 gm / min., resulting to
loss of electrical function
o another one at 10ml / 100 gm / min,
resulting to loss of cell polarizaton.
PENUMBRA
Heterogeneity in brain injury has been
documented in an infarcted zone. Blood flow to an
infarcted zone is said to have:
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o a central region or core of very low
flow that results in rapid cell demise and
o a peripheral penumbra where decline
in blood declines in flow is more
moderate and cell death is not
immediate.
The penumbra is thought to represent
salvageable tissues that may go on to infarction.
If blood flow is normalized at an adequate time,
the brain cells will normalize.
Imaging in stroke
• Most commonly used imaging method non-
contrast CT scan but MRI is fast catching-up.
• CT scan is commonly used in stroke due to:
- Widespread and ready availability
- Ease of hemorrhage detection
- Compatibility with monitoring equipment
- Rapid scanning techniques for unstable
patients.
Emergent evaluation in Acute Stroke:
• Goals:
- Confirm cause of deficit is stroke
related.
- Assess possible reversibility of the
lesion.
- Determine most likely etiology.
- Predict likelihood of immediate
complications.
- Begin appropriate treatment.
• Opportunities for Intervention:
- Before any clinical symptoms
- After transient ischemic attack or minor
stroke.
- During acute ischemic stroke
- Before a recurrence.
Imaging Signs of Hyperacute Infraction:
• Hyperdense LMCA sign
• Loss of gray-white matter differentiation
• Sulcal effacement
• Loss of insular ribbon
• Obscurred lentiform nucleus.
Lacunar Infarction:
• Not larger than 1.5 cm
• Deep gray matter
• Brain stem
• Deep hemispheric white matter
• Supplied by perforators
Cardioembolic Infarction
• Relative stasis resulting to mural thrombus, ex.:
M.I., atrial fib., ventricular aneurysm
• Valvular heart disease resulting to vegetation or
from prosthesis
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• Cardiac tumors the CT scanner is the most accurate but this would
• Congenital HD, ex.: right to left shunt depend on the cooperation of the facility operators.

Watershed Infarction  Once the patient data is deleted from the memory
• Boundary zone infarct file of the system, the direct volume measurement can
no longer be applied on the data in the hard copy
• Internal carotid stenosis or occlusion
(film).
• Systemic hypotension
• Embolic events
 In older model CT Scan where volume
measurement is not available, an alternative method
Hemorrhagic Infarction:
is possible by using the area of the hemorrhage:
• Hemorrhagic transformation results to petechial Volume in cubic cm =
hemorrhage or frank hematoma Area x slice thickness (millimeters) 1000
• Anticoagulant therapy
• Thrombolytic agents ABC/2 Method
• More common in cardioembolic strokes • Kothari, et. al., has developed a simple bedside
• Larger cardioembolic strokes are more likely to method of ICH volume determination with the
bleed following formula:
ICH volume = (A x B x C)/ 2
Temporal Evolution of Infarction on CT Scan:
0 – 4 hrs. Normal to subtle hypodensity
± sulcal effacement
• Step 1: The largest dimension of the
hemorrhage is determined in the
1 – 7 days Mass effect peaks at 3 – 4 days
series of CT slices, then the largest diameter of
the hematoma is measured and labeled – A
1 – 8 weeks Contrast enhancement
Days to Hypodensity • Step 2: On the same slice, the largest diameter
months/ yrs of hemorrhage 90o to A is determined and
Weeks to Atrophy labeled – B.
years • Step 3: “C” or the cephalocaudal dimention of
the hemorrhage is determined by comparing the
Acute to Subacute Infarction Changes: rest of the CT slices to the largest hemorrhage on
• Vasogenic Edema that later on wanes the scan.
• Enhancement -(Luxury perfusion) o If the hemorrhage area is 75 % of the
• Petechial hemorrhage largest hemorrhage area =
one (1) slice for determining C
Hypertensive Hemorrhage o If the area was 25 to 75% of the slice
• In hypertensives, hyalinization within the walls of where the hemorrhage was largest, the
small cerebral vessels results in slice is considered as one-half a
Microaneurysms hemorrhage slice
that are less than 1.0 mm in size, o If the area was less than 25 % of the
(Charcot & Bouchard), largest hemorrhage, this is not
that tend to arise from perforating vessels that considered as a hemorrhage slice.
will later on bleed.

Some of the Causes of ICH:  When the CT slice thickness is smaller than
Hypertension the table movement, as will be commonly
Amyloid Vasculopathy encountered in CT slices of the posterior fossa,
Aneurysm there will necessarily be the presence of inter-
A-V malformation slice gaps.
Neoplasm
Coagulation disorders, e.g. hemophilia  To remedy this, use the table movement
Aticoagulants measurement for thickness of the slice instead of
Vasculitis the actual slice thickness to calculate for volume.
Drug abuse e.g. cocaine
Trauma (A x B x C ) ÷ 2 = Volume in cc
Idiopathic A = 4.0 cm
B = 2.6 cm
• Hypertension accounts for 40-50% of deaths from C = 2.5 cm
non-traumatic hemorrhage in an autopsy series.
• In young (less than 40 y/o) normotensive (4.0 x 2.6 x 2.5) ÷ 2 = 13 cc
patients, cause remains unknown but cryptic
AVM is a suspect. Actual computation directly done in the CT scan = 13.3 cc

Why is there a need to measure hemorrhage size?

• Volume of the hemorrhage is a strong indicator Reader No. Intraclass Difference P† Mean Time per
of the 30 day survival of the patient. Correlation From Measurement,‡ s
Planimetric,*
Methods of measuring ICH Volume: cm3
1 (Neurosurgery 20 .99 -2.0 ± 1.2 .11 35
• Direct volume measurement in the CT Scan faculty)
system or in a work station 2 (Neurosurgery 20 .99 0.6 ± 3.0 .85 40
• Planimetry resident)
• Application of the formula for the sphere: 3 (Emergency 20 .99 0.8 ± 1.3 .55 33
Volume = 4/3 π (r)3 physician)
• ABC/2 method 4 (Nurse) 20 .99 -2.5 ± 1.5 .07 31
Reliability & Reproducibility of the ABC/2 Method of
 Among different methods of volume Measuring Intraparenchymal Hemorrhage Volume
measurements, the direct volume measurement in Interrater reliability (readers 1-4): Interclass correlation = .99
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Intrarater reliability (reader 3): Interclass correlation = .99 (P=.19)

* Mean±SE difference from planimetric measurement.

† Difference from planimetric measurement.
‡ Mean time to determine hemorrhage volume per CT
scan with the ABC/2 technique

Mean Hemorrhage Volumes

Temporal Evolution of ICH Hemorrhage Volume,

cm3
Biochemical Clinical Approximate Intens Intensi Location No. Planimetric ABC/2 R2
Form Stage Time of ity on ty on Deep 83 23.0 ± 2.7 23.5 ± 2.9 .94
Appearance T1WI T2WI
OxyHg in Hyper- Immediately to Lobar 21 44.6 ± 8.4 49.9 ± 9.9 .96
RBCs acute first several ≈ á Brain Stem 8 13.6 ± 7.2 12.3 ± 6.3 .99
hours Cerebellar 6 19.6 ± 4.3 24.4 ± 5.9 .78
DeoxyHg in Acute Hours to days Total 118 26.0 ± 2.6 27.5 ± 2.9 .96
≈, â ââ
RBCs Hemorrhage volumes are mean ± SE.
MetHg in Early First several
RBCs subacut days áá ââ
e
Extracellular Subacut Days to
MetHg e to months áá áá
chronic
Ferritin and Remote Days to
Hemosiderin indefinitely ≈, â ââ

Acute Infarction findings in MRI:

• Lesion in arterial distribution
• High intensity in Proton density or in T2 FLAIR
• Gyral swelling / sulcal effacement
• Absent arterial flow void
• Subcortical white matter hypointensity
• Intravascular contrast enhancement

Diffusion weighted imaging:

• Signal attenuation is noted in areas of free
diffusion
• Signal intensity is increased in areas of restricted
diffusion with decrease in apparent diffusion
coefficient in brain tissue
• Decrease in diffusion of water in early ischemia is
due to shift of water from extracellular to
intracellular

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