Diagnostic Imaging Methods in Central Nervous System Disorders

P. Danilo J. Lagamayo, MD

Headache:Primary:

MigraineClusterTension

Secondary:Increased Intracranial Pressure:

NeoplasmsAbscessGranulomas

Meningeal Irritations:MeningitisSubarachnoid Hemorrhage

Vascular Disorders:StrokeMalformationsArteritis

Head Trauma:ConcussionHematoma

Other Cranio-Facial Pains:Trigeminal Neuralgia

Incidence of Primary Brain Tumors:

- 6 persons / 100,000 population / year

- about 1 in 12 primary brain tumors occur in children under 15 years old.

Clinical Presentation of Brain Tumors:

Focal neurologic deficitIncrease intracranial

pressure: - Headache that is more severe in AM

- Nausea / Vomiting- Diplopia - Papilledema

- Ontundation & Lethargy (ominous) Focal neurologic signs and symptoms:

- seizure, seen in about ½ of patients

Clinical Presentation of Brain Tumors: (II) Non-localizing findings: - fatigue

- malaise- impotense

- glactorrhea - growth failure

- macrocephaly in young children

Pathological Classification of Intracranial Tumors:

Neuroepithelial:Astrocytes -

AstrocytomaOligodendrocytes - Oligodendroglioma

Ependymal cells & Choroid Plexus-

Ependymoma Choroid Plexus Papilloma Neurons -

Gangliomas, Gangliocytomas,

NeuroblastomasPineal cells - Pineocytomas

PineoblastomasPoorly differentiated

Glioblastoma multiforme and embryonic cells Medulloblastoma

Pathological Classification of Intracranial Tumors: (cont.)

Meninges - MeningiomaNerve sheet cells -

Neuroma- Neurofibroma Blood

vessels - HemangioblastomasGerm cells - Germinoma

- TeratomaTumors of malde-velopmental origin -

Craniopharyngioma- Epidermoid/Dermoid

cyst- Colloid cysts

Pathological Classification of Intracranial Tumors:

Anterior pituitary gland- Pituitary adenoma- Adenocarcinoma

Local extension - Chordoma from adjacent - Glomus jugulare tumors - Chondroma

- Chondrosarcoma - Cylindroma

Incidence of Tumors:Glioblastoma - - - - - - - - -

55% Astrocytoma - - - - - - - - - 20.5% Ependymoma - - - - - - - - 6% Medulloblastoma - - - - - - 6% Oligodendroglioma _ - - -

5% Choroid Plexus Papilloma 2%

Other less common entities:Neuronal tumors –

Gangliocytomas, ganglioglioma Embryonal – PNET Pineal Region – germ cellPrimary CNS Lymphoma

Primary Imaging Methods for Diagnosis of CNS tumors:

- MRI

- CT scan

- Angiography

Advantages of CT Scan

- Wide availability;

- Can accommodate life support systems;

- Fast imaging methods

- Can show bone structures and their pathologic changes like fractures;

- Cheap.

Disadvantages of CT Scan

• Cannot demonstrate soft tissue detail of the sella turcica, the brain stem and the cerebellum;

• Not very sensitive to white matter lesions;

• Cannot differentiate encephalomacic lesions of hemorrhage from infarcts;

• Uses ionizing radiation and cannot be used on pregnant patients.

Advantages of MRI

• Unaffected by the thick bone encasement of the calvarium in the posterior fossa and the sellar turcica;

• Accurate determination of the age and evidence of hemorrhage;

• More sensitive for detection of white matter lesion;

• Ability to perform multiplanar imaging;• Does not use radiation and can be safely used

on pregnant patients.

Disadvantages of MRI

• Longer time needed to complete an examination;

• Needs patient cooperation, e.g. patient must not move during an imaging sequence that can take anywhere from 1 minute to as long as 7 minute;

• Any metal implement is not allowed into the MR room.

Disavantages of MRI

• Cannot image patients with:– Pacemakers– Neurostimulators– Newly applied vascular clips – Vacular clips with ferromagnetic materials

(steel or iron)– Metal foreign bodies in the orbit– Claustrophobic patients– Patients who need extensive life support

Causes of Low Signal Intensity in Tumors in T2WI:

Paramagnetic effects- Iron with dystrophic Ca or

necrosis - Ferritin/hemosiderin from prior bleed

- Deoxy hgb in acute bleed- Intracellular met hgb in

early subacute bleed - Melanin (or other free radicals)

Causes of Low Signal Intensity in Tumors in T2WI (cont.):

Low spin density - Calcifications

- Scant cytoplasm (high nucleus:cytoplasm ratio)

- Dense CellularityFibrocollagenous stroma

Macromolecule content Very high (non-paramagnetic) protein content

Intratumoral vessels - Signal void from

rapid flow

Causes of High Signal Intensity in Tumors in T1WI:

Paramagnetic effects from hemorrhage- Subacute – chronic

blood (met hgb) Paramagnetic materials w/out hemorrhage - Melanin - Naturally occuring ions associated with

necrosis of calcification:Manganese, Iron, CopperNon-paramagnetic effects

- Very high (non-paramagnetic) proteins - Fat - Flow related enhancement in tumor vessels

Requirements for contrast enhancement:

- absence of blood-brain barrier- adequate delivery of

contrast material - extracapillary interstitial space to accommodate contrast

- appropriate contrast dosage- spatial resolution

- imaging parameters to allow contrast detection

- time for contrast to accumulate in the region

of interest

Mechanism for contrast enhancement in CNS tumors:

Formation of capillaries with deficient blood-brain barrier rather than the destruction of blood-barrier is presumed as the mechanism for tumor enahcement.

The capillaries of metastatic tumors to the brain has no blood-brain barrier since these tumors come from elsewhere and not from the brain.

Type of enhancement:- immediate or delayed

- evanescent or persistent - dense and homogenous - minimal or irregular

Note: Lack of tumor enhancement do not signify lack of tumor.

Effects of Tumor Necrosis on Signal Intensity:

Short relaxation times HemorrhageLiberation of

cellular iron Release of free radicalsProteinaceous debris

Prolong relaxation Cystic change with increased times water

Frequently Cystic TumorsColloid cystCraniopharyngiomaDesmoplastic infantile gangliomaDermoidEpendymoma (supratentorial and spinal)EpidermoidGanglion cell tumorsGlioblastoma (cystic necrosis)HemangioblastomaPilocytic astrocytomaPleomorphic xanthoastrocytomaRathke cleft cyst

Magnetic Resonance Criteria for Cystic LesionsMorphology Sharply demarcated, round

smooth

Signal Intensity Isointense to cerebrospinal fluid on all spin echo images (tumor cysts can be hyperintense due to ↓ T1)

Fluid-debris levels (bleed into necrotic or cystic regions)

Intracellular blood-cyst fluid Intracellular blood-extracellular blood

Motion of intra- lesional fluid

Lesion emanates ghost images along phase-encoding axis

Intralesional signal loss (especially on steady-state sequences)

Hemorrhagic TumorsPrimary brain tumors

Glioblastoma/anaplastic asctrocytomaAnaplastic oligodendroglioma/oligodendrogliomaEpendymomaTeratoma

Metastatic diseaseMelanomaRenal cell carcinomaChoriocarcinomaLung carcinomaBreast carcinomaThyroid carcinoma

Intratumoral Hemorrhage vs. BenignIntracranial Hematomas

Intratumoral hemorrhage:

- Markedly heterogenous, related to: Mixed stages of blood Debris-fluid (intracellular-extracellular blood) levels Edema + tumor + necrosis with blood

- Identification of nonhemorrhagic tumor component- Delayed evolution of blood breakdown products- Absent, diminished, or irregular ferritin/hemosiderin -Persistent surrounding high intensity on long TR images (i.e., tumor/edema) and mass effect, even in late stages

Intratumoral Hemorrhage vs. Benign Intracranial HematomasBenign hemorrhage:

- Shows expected signal intensities of acute, subacute or chronic blood, depending on stage of hematoma

- No abnormal nonhemorrhagic mass- Follows expected orderly progression- Regular complete ferritin/hemosiderin rim- Complete resolution of edema and mass effect in chronic stages

Intratumoral Melanin vs. Hemorrhage

Signal intensity

(relative to gray matter)

T1-weighted

Image

T2-weighted

Image

Amelanotic tumor

Melanotic tumor

Early subacute blood

(intracellular methemoglobin)

Late subacute blood

(extracellular methemoglobin)

↓

↑↑

↑↑

↑↑

sl. ↑

= or sl. ↓

↓↓

↑↑

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 NeoplasmsAstrocytoma Anaplastic astrocytoma

Typical site(s) of origin

Signal intensity

characteristics(on

T2-weighted image)

Vascular flow voids

Contrast

enhancement

Prognosis (median survival, if available)

Cerebral hemisphere

(adult)

Brainstem (child)

Cerebellum (young adult)

Homogeneous; high

intensity

Not seen

Variable; irregular

7-8 yr

Cerebral hemisphere

(adult)

Brainstem (child)

Some heterogeneity

Unusual

Common; irregular

2-3 yr

Glioblastoma Gliomatosis

Typical site(s) of origin

Signal intensity

characteristics(on

T2-weighted image)

Vascular flow voids

Contrast

enhancement

Prognosis (median survival, if available)

Cerebral hemisphere

(adult)

Markedly heterogeneous;

hemorrhage and

necrosis common

Common

Common; irregular

12 mo

Cerebral hemisphere (young

or middle-aged adult)

Ill-defined; high intensity

Rare

Uncommon

Estimated as months

Diffuse Astrocytic Brain Neoplasms

Pediatric Supratentorial Hemispheric Neoplasms

Juvenile pilocytic astrocytoma

Ganglioglioma

Signal intensity

characteristics (on

T2-weighted image)

Contrast

enhancement

Hemorrhage

Calcification

Prognosis

Sharply demarcated;

commonly cystic

Common; dense

Rare

Uncommon

Excellent

Sharply demarcated;

commonly cystic

Common; irregular

Rare

Common

Excellent

Pleomorphic xanthoastrocytoma

Embryonal tumor

(e.g., cerebral neuroblastoma)

Signal intensity

characteristics (on

T2-weighted image)

Contrast

enhancement

Hemorrhage

Calcification

Prognosis

Sharply demarcated

with subjacent cyst

Common in solid

portion

Rare

Uncommon

Variable

Markedly

heterogeneous

Common; irregular

Common

Common

Poor

Pediatric Supratentorial Hemispheric Neoplasms

DNT

Signal intensity

characteristics (on

T2-weighted image)

Contrast

enhancement

Hemorrhage

Calcification

Prognosis

Sharply demarcated

heterogeneous

Unknown

Rare

Common

Excellent

Pediatric Supratentorial Hemispheric Neoplasms

Tumor type Typical location

Central neurocytoma

Ependymoma

Subependymoma

Oligodendroglioma

Pilocytic astrocytoma

Meningioma

Choroid plexus tumor

Epidermoid

Subependymal giant cell

astrocytoma

Colloid cyst

Arachnoid cyst

Lateral (attached to septum pellucidum)

Fourth, lateral

Lateral, fourth

Lateral

Lateral, third, or fourth

Lateral (atrium)

Lateral (atrium) or third in children, fourth in adults

Any ventricle

Lateral

Third

Any ventricle

Intraventricular Masses

Tumor type Intensity characteristics on T2-weighted images

Contrast enhancement

Central neurocytoma

Ependymoma

Subependymoma

Oligodendroglioma

Pilocytic astrocytoma

Meningioma

Choroid plexus tumor

Epidermoid

Subependymal giant cell astrocytoma

Colloid cyst

Arachnoid cyst

Isointense to gray matter

Heterogeneous

Hyperintense to gray matter

Heterogeneous

Hyperintense to gray matter

Isointense to gray matter

Heterogeneous

Slightly hyperintense to CSF

Hyperintense to gray matter

Hyperintense to gray matter

Usually dense

Heterogeneous

None

Variable; irregular

Dense

Dense

None

Generally enhance

Limited enhancement at periphery

None

Isointense to CSF

Intraventricular Masses

Juvenile pilocytic astrocytoma

Medulloblastoma

Signal intensity

characteristics (on T2-WI)

Contrast enhancement

Calcification

Hemorrhage

Tendency to seed

CSF pathways

Prognosis (estimated survival)

Sharply demarcated;

commonly cystic

Common in solidportion (mural nodule)

Uncommon

Rare

Extremely low

>90% 10-yr survival

Homogeneous; low to

moderate intensity

Common; dense

Uncommon

Uncommon

High

50% 5-yr survival

Posterior Fossa Tumors in Childhood

Ependymoma Diffuse pontine glioma

Signal intensity

characteristics

(on T2WI)

Contrast

enhancement

Calcification

Hemorrhage

Tendency to seed

CSF pathways

Prognosis (estimated

survival)

Markedly heterogeneous

Common; irregular

Common

Common

Low to moderate

65-70% 5-yr survival

Ill-defined; high intensity

Variable

Rare

Common

Low

<1-2% 5-yr survival

Posterior Fossa Tumors in Childhood

Pineal Region TumorsGerminoma Teratoma Pineoblastoma

Age; sex predilection

Pineal vs.

parapineal

Signal intensity

(heterogeneous

vs.

homogeneous)

Hemorrhage

Calcification

Brain edema or

invasion

Tendency to

metastasize

Enchancement

Prognosis

Child; male

Pineal

Homogeneous

(but often

hemorrhagic)

Common

Rare

Common

Yes

Dense

Excellent

Child; male

Pineal

Strikingly

heterogeneous

Typical

Typical

Variable

Variable

Variable

Variable

Child; none

Pineal

Homogeneous

(unless

hemorrhagic)

Common

Common

Common

Yes

Dense

Poor

Pineal Region TumorsPineocytoma Glioma Meningioma

Age; sex

predilection

Pineal vs.

parapineal

Signal intensity

(heterogeneousvs.

homogeneous)

Hemorrhage

Calcification

Brain edema or

invasion

Tendency to

metastasize

Enchancement

Prognosis

Adult; none

Pineal

Variable

Common

Common

Uncommon

No

Dense

Variable

Child; none

Parapineal

(usually)

Homogeneous

(usually)

Rare

Common

Primarily

midbrain

Variable

Variable

Variable

Adult; none

Parapineal

(usually)

Homogeneous

Rare

Common

Occasional

No

Dense

Excellent

Magnetic Resonance Findings in Extraaxial Mass Lesions

Suggestive Definitive

Peripheral, broadly based

along calvarium

Overlying bone changes

Enhancement of adjacent

meninges

Displacement of brain from

skull

Cerebrospinal fluid cleft between

brain and lesion

Vessels interposed between brain

and lesion

Cortex between mass and

(edematous) white matter

Dura (meninges) between

(epidural) mass and brain

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 syndrome 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 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 Normal Brain:

The threshold for cerebral ischemia is approximately at:

23 ml / 100 g /min.

The Normal Brain:

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:

1. Large Artery or Atherosclerotic Infarction

2. Cardioembolic Infarction 3. Small Vessel Infarction 4. 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.

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.

The Abnormal Brain:

Blood flow values below:

10 ml / 100 gm / min.,

may lead to infarction within a few minutes.

The Abnormal Brain:

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, one occurring at blood

flow range of 15-20 ml / 100 gm / min., resulting to loss of electrical function and another one at 10ml /

100 gm / min. , resulting to loss of cell polarizaton.

PENUMBRAHeterogeneity in brain injury has been documented in an infarcted zone.

Blood flow to an infarcted zone is said to have: A. a central region or core of very low flow that results in rapid cell demise and B. a peripheral penumbra where decline in flow is more moderate and cell death is not immediate.

PENUMBRAThe 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.

Emergent Evaluation in Acute Stroke:

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:

1. Hyperdense LMCA sign2. Loss of gray-white matter differentiation3. Sulcal effacement.4. Loss of insular ribbon.5. 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 - Cardiac tumors - Congenital HD, ex.: right to left shunt

Watershed Infarction:

- Boundary zone infarct - Internal carotid stenosis or occlusion - Systemic hypotension - Embolic events

Hemorrhagic Infarction:

- Hemorrhagic transformation results to petechial hemorrhage or frank hematoma - Anticoagulant therapy

- Thrombolytic agents - More common in cardioembolic strokes - Larger cardioembolic strokes are more

likely to bleed

Temporal Evolution of Infarction on CT Scan: 0 – 4 hrs. Normal to subtle hypodensity

± sulcal effacement

1 – 7 days Mass effect peaks at 3 – 4 days

1 – 8 weeks Contrast enhancement

Days to Hypodensity months/ yrs

Weeks to years Atrophy

Acute to Subacute Infarction Changes:

1. Vasogenic Edema that later on wanes

2. Enhancement - (Luxury perfusion)

3. Petechial hemorrhage

Hypertensive Hemorrhage

In hypertensives, hyalinization within the walls of small cerebral vessels results in

microaneurysms that are less than 1.0 mm in size,

(Charcot & Bouchard), that tend to arise from perforating vessels that will later on bleed.

Some of the Causes of ICH:HypertensionAmyloid VasculopathyAneurysmA-V malformationNeoplasmCoagulation disorders, e.g.

hemophiliaAticoagulantsVasculitisDrug abuse e.g. cocaineTraumaIdiopathic

Hypertension accounts for 40-50% of deaths from non-traumatic hemorrhage in an autopsy series.

In young (less than 40 y/o) normotensive patients, cause remains unknown but cryptic AVM is a suspect.

Why is there a need to measure hemorrhage size?

Volume of the hemorrhage is a strong indicator of the 30 day survival of the patient.

Methods of measuring ICH Volume:

A. Direct volume measurement in the CT Scan system or in a work station;

B. PlanimetryC. Application of the formula for

the sphere:

Volume = 4/3 (r)3

D. ABC/2 method

Among different methods of volume measurements, the direct volume measurement in the CT scanner is the most accurate but this would depend on the cooperation of the facility operators.

Once the patient data is deleted from the memory file of the system, the direct volume measurement can no longer be applied on the data in the hard copy (film).

In older model CT Scan where volume measurement is not available, an alternative method is possible by using the area of the hemorrhage:

Volume in cubic cm =

Area x slice thickness (millimeters) 1000

ABC/2 Method:

Kothari, et. al., has developed a simple bedside method of ICH volume determination with the following formula:

ICH volume = A x B x C2

ABC/2 Method (continued):Step 1: The largest dimension of the

hemorrhage is determined in the series of CT slices, then the largest diameter of the hematoma is measured and labeled - A;

Step 2: On the same slice, the largest diameter of hemorrhage 90o to A is determined and labeled – B.

ABC/2 Method (continued):Step 3: “C” or the cephalocaudal

dimention of the hemorrhage is determined by comparing the rest of the CT slices to the largest hemorrhage on the scan.

If the hemorrhage area is 75 % of the largest hemorrhage area = one (1) slice for determining C;

ABC/2 Method (continued):Step 3: If the area was 25 to 75% of the

slice where the hemorrhage was largest, the slice is considered as one-half a hemorrhage slice;

If the area was less than 25 % of the largest hemorrhage, this is not considered as a hemorrhage slice.

When the CT slice thickness is smaller than the table movement, as will be commonly encountered in CT slices of the posterior fossa, there will necessarily be the presence of inter-slice gaps.

To remedy this, use the table movement measurement for thickness of the slice instead of the actual slice thickness to calculate for volume.

1 2

3 4

A

B

(2)

“1” slice

ABC/2 Method:

(A x B x C ) ÷ 2 = Volume in ccA = 4.0 cmB = 2.6 cmC = 2.5 cm

(4.0 x 2.6 x 2.5) ÷ 2 = 13 cc

Actual computation directly done in the CT scan = 13.3 cc

Reader No. Intraclass Correlatio

n

Difference From Planimetric,*

cm3

P† Mean Time per Measurement,‡

s

1 (Neurosurgery faculty)

20 .99 -2.0 ± 1.2 .11 35

2 (Neurosurgery resident)

20 .99 0.6 ± 3.0 .85 40

3 (Emergency physician)

20 .99 0.8 ± 1.3 .55 33

4 (Nurse) 20 .99 -2.5 ± 1.5 .07 31Interrater reliability (readers 1-4): Interclass correlation = .99Intrarater 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

Reliability & Reproducibility of the ABC/2 Method of Measuring Intraparenchymal Hemorrhage Volume

Hemorrhage Volume, cm3

Location No. Planimetric ABC/2 R2

Deep 83 23.0 ± 2.7 23.5 ± 2.9 .94

Lobar 21 44.6 ± 8.4 49.9 ± 9.9 .96

Brain Stem

8 13.6 ± 7.2 12.3 ± 6.3 .99

Cerebellar 6 19.6 ± 4.3 24.4 ± 5.9 .78

Total 118 26.0 ± 2.6 27.5 ± 2.9 .96

Hemorrhage volumes are mean ± SE.

Mean Hemorrhage Volumes

Temporal Evolution of ICH

Biochemical Form

Clinical Stage Approximate Time of Appearance

OxyHg in RBCs HyperacuteImmediately to first several hours

DeoxyHg in RBCs

Acute Hours to days

MetHg in RBCs Early subacute First several days

Extracellular MetHg

Subacute to chronic

Days to months

Ferritin and Hemosiderin

Remote Days to indefinitely

Biochemical Form

Intensity on T1WI

Intensity on T2WI

OxyHg in RBCs

DeoxyHg in RBCs

,

MetHg in RBCs Extracellular metHg

Ferritin and hemosiderin

,

Temporal Evolution of ICH

Acute Infarction findings in MRI:

1. Lesion in arterial distribution 2. High intensity in Proton density or in T2 FLAIR

3. Gyral swelling / sulcal effacement 4. Absent arterial flow void 5. Subcortical white matter hypointensity 6. 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