ct koass michel

8/7/2019 ct koass michel

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A. Orbit

B. Sphenoid Sinus

C. Temporal Lobe

D. External AuditoryCanal

E. Mastoid Air Cells

F. Cerebellar

Hemisphere


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A. Frontal Lobe B. Frontal Bone

(Superior Surface ofOrbital Part)

C. Dorsum Sellae D. Basilar Artery E. Temporal Lobe F. Mastoid Air Cells G. Cerebellar

Hemisphere


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A. Frontal Lobe B. Sylvian Fissure

C. Temporal Lobe D. Suprasellar Cistern E. Midbrain F. Fourth Ventricle G. Cerebellar

Hemisphere


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A. Falx Cerebri B. Frontal Lobe

C. Anterior Horn of Lateral Ventricle D. Third Ventricle E. Quadrigeminal Plate Cistern

F. Cerebellum


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A. Anterior Horn of the LateralVentricle

B. Caudate NucleusC. Anterior Limb of the Internal

CapsuleD. Putamen and Globus PallidusE. Posterior Limb of the Internal

CapsuleF. Third Ventricle

G. Quadrigeminal Plate Cistern

H. Cerebellar VermisI. Occi ital Lobe


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A. Genu of the CorpusCallosum

B. Anterior Horn of the

Lateral Ventricle C. Internal Capsule D. Thalamus E. Pineal Gland F. Choroid Plexus G. Straight Sinus


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A. Falx Cerebri B. Frontal Lobe C. Body of the Lateral

Ventricle

D. Splenium of theCorpus Callosum

E. Parietal Lobe F. Occipital Lobe G. Superior Sagittal

Sinus


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A. Falx Cerebri

B. Sulcus

C. Gyrus

D. SuperiorSagittal Sinus


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Skull Fractures

Linearskull

fractureof therightparietalbone(arrows


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Klasifikasi :

1. Cidera kepala langsung : akibat langsung trauma. Extracranial : Scalp & skull

Intracranial : extra-axial : EPH, SDH, SAH

intra-axial : lesi-lesi intra-axial, diffuse axonal injury, kontusi

kortikal, perdarahan intraventrikel

2. Cidera kepala sekunder: manifestasi klinis sering kalilebih parah : edema cerebral diffus, effek massa denganherniasi cerebral, anoxia/hypoxia, infark & hemorrhage

sekunder, infeksi dll.


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Mekanisme Cidera Kepala

1. Non-penetrating trauma :

Effekt trauma ditentukan oleh : Arah, type & kekuatan ( compression, torsion & axonal shearing

stresses )

Karakter struktural dari skull & struktur intracranial : pemukaan tidak rata : orbita, petrous bones

pembagian kompartemental : falx, tentorium -> herniasi

struktur otak sendiri : coup, contre coup.

2. Penetrating trauma :

trauma disebabkan oleh benda tajam atau peluru


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Skull fractures are categorized as linearordepressed, depending on whether thefracture fragments are depressed below thesurface of the skull.

Linear fractures are more common.

The bone windows must be examinedcarefully.

A skull fracture is most clinically

significant if the paranasal sinus or skullbase is involved.


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Fractures must be distinguished fromsutures that occur in anatomical locations(sagittal, coronal, lambdoidal) and venouschannels.

Sutures have undulating margins both

sutures & venous channels have scleroticmargins.

Venous channels have undulating sides.

Depressed fractures are characterized byinward displacement of fracture fragments.


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Subarachnoid

Hemorrhage

High densityblood(arrowheads)fills the sulciover theright cerebral

convexity inthissubarachnoidhemorrhage.


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A subarachnoid hemorrhage occurs with injury ofsmall arteries or veins on the surface of the brain.

The ruptured vessel bleeds into the space betweenthe pia and arachnoid matter.

The most common cause of subarachnoidhemorrhage is trauma. In the absence of significanttrauma, the most common cause of subarachnoidhemorrhage is the rupture of a cerebral aneurysm.

When traumatic, subarachnoid hemorrhage occursmost commonly over the cerebral convexities oradjacent to otherwise injured brain (i.e. adjacent to acerebral contusion).


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If there is a large amount of subarachnoidhemorrhage, particularly in the basilarcisterns, the physician should considerwhether a ruptured aneurysm lead to thesubsequent trauma.

Cerebral angiography may be needed for

further evaluation. On CT, subarachnoidhemorrhage appears as focal high density insulci and fissures orlinear hyperdensity in thecerebral sulci.

Again, the most common location ofposttraumatic subarachnoid hemorrhage is overthe cerebral convexity. This may be the onlyindication of cerebral injury.


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Acute Subdural Hematoma

High density,crescent shapedhematoma(arrowheads)

overlying theright cerebralhemisphere.

Note the shift of

thenormally midlineseptumpellucidum dueto the mass

effect arrow.


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Deceleration and acceleration or rotationalforces that tear bridging veins can cause anacute subdural hematoma.

The blood collects in the space between thearachnoid matter and the dura matter.

The hematoma on CT has the followingcharacteristics:- Crescent shaped

- Hyperdense, may contain hypodensefoci due to serum, CSF or active

bleeding.

- Does not cross dural reflections


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The hypodense region (arrow) within thehigh densityhematoma (arrowheads) may indicateactive bleeding


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Subacute Subdural

Hematoma

Subacutesubduralhematoma

(arrowheads).Note thecompression ofgray and white

matter in theleft hemispheredue to themass effect.


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Subacute SDH may be difficult to visualize by CTbecause as the hemorrhage is reabsorbed it becomesisodense to normal gray matter.

A subacute SDH should be suspected when youidentify shift of midline structures without an obviousmass.

Giving contrast may help in difficult cases because theinterface between the hematoma and the adjacent

brain usually becomes more obvious due toenhancement of the dura and adjacent vascularstructures.

Some of the notable characteristics of subacute SDHare:- Compressed lateral ventricle- Effaced sulci- White matter "buckling"- Thick cortical "mantle"


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Chronic Subdural

Hematoma

Crescent shapedchronic subduralhematoma

(arrowheads).Noticethe lowattenuation due toreabsorbtion ofthe hemorrhageover time.


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Chronic SDH becomes low density as thehemorrhage is further reabsorbed. It isusually uniformly low density but may beloculated. Rebleeding often occurs andcauses mixed density and fluid levels.


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This chronicsubduralhematoma

(arrowheads)showsthe septationsand loculationsthat oftenoccur overtime.


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Epidural

Hematoma

Biconvex(lenticellular)epiduralhematoma(arrowheads),

deep to theparietal skullfracture

(arrow).


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An epidural hematoma is usually associatedwith a skull fracture.

It often occurs when an impact fractures thecalvarium.

The fractured bone lacerates a dural artery oravenous sinus.

The blood from the ruptured vessel collectsbetween the skull and dura.


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On CT, the hematoma forms a hyperdensebiconvex mass.

It is usually uniformly high density but maycontain hypodense foci due to active bleeding.

Since an epidural hematoma is extradural it cancross the dural reflections unlike a subduralhematoma.

However an epidural hematoma usually doesnot cross suture lines where the dura tightlyadherens to the adjacent skull.


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Diffuse Axonal

Injury

Hemorrhage ofthe posteriorlimb of the

internalcapsule(arrow) andhemorrhage of

the thalamus(arrowhead).


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Diffuse axonal injury is often referred to as "shearinjury".

It is the most common cause ofsignificant morbidityin CNS trauma.

Fifty percent of all primary intra-axial injuries arediffuse axonal injuries.

Acceleration, deceleration and rotational forces causeportions of the brain with different densities to moverelative to each other resulting in the deformation andtearing of axons.


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Immediate loss of consciousness is typical of theseinjuries.

The CT of a patient with diffuse axonal injury may be

normal despite the patient's presentation with a profoundneurological deficit. With CT, diffuse axonal injury mayappear as ill-defined areas of high density orhemorrhagein characteristic locations.

The injury occurs in a sequential pattern of locationsbased on the severity of the trauma.

The following list of diffuse axonal injury locations isordered with the most likely location listed first followed by

successively less likely locations:- Subcortical white matter- Posterior limb internal capsule- Corpus callosum- Dorsolateral midbrain


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Hemorrhage in the corpus callosum(arrow).


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Cerebral

Contusion

Multiple foci ofhigh densitycorresponding to

hemorrhage(arrows) in anarea of lowdensity

(arrowheads) inthe left frontallobe due tocerebral

contusion.


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Cerebral contusions are the most commonprimary intra-axial injury.

They often occur when the brain impacts an

osseous ridge or a dural fold.

The foci of punctate hemorrhage or edema arelocated along gyral crests.


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The following are common locations:- Temporal lobe - anterior tip, inferior surface,sylvian region.

- Frontal lobe - anterior pole, inferior surface- Dorsolateral midbrain- Inferior cerebellum

On CT, cerebral contusion appears as an ill-definedhypodense area mixed with foci of hemorrhage.

Adjacent subarachnoid hemorrhage is common. After24-48 hours, hemorrhagic transformation orcoalescence ofpetechial hemorrhages into a roundedhematoma is common.


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Intraventricular Hemorrhage

Intraventricularhemorrhage(arrow) found in a

traumapatient. Note thesubarachnoidhemorrhage in the

sulci in thesubarachnoidspace(arrowheads).


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Traumatic intraventricular hemorrhage isassociated with diffuse axonal injury, deepgray matter injury, and brainstemcontusion. An isolated intraventricularhemorrhage may be due to rupture ofsubependymal veins.


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S k S b


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Stroke Subtypes

Strokes are classified into two major types -hemorrhagic and ischemic.

Hemorrhagic strokes are due to rupture of acerebral blood vessel that causes bleeding into or

around the brain. Hemorrhagic strokes account for16% of all strokes. An ischemic stroke is caused byblockage of blood flow in a major cerebral bloodvessel, usually due to a blood clot. Ischemic strokes

account for about 84%

of all strokes. Ischemic strokesare further subdivided based on their etiology intoseveral different categories including thromboticstrokes, embolic strokes, lacunar strokes andhypoperfusion infarctions.


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Hemorrhagic Stroke


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Hemorrhagic strokes account for16% of allstrokes.

There are two majorcategories of hemorrhagicstroke.

Intracerebral hemorrhage is the mostcommon, accounting for10% of all strokes.

Subarachnoid hemorrhage, due to rupture ofa cerebral aneurysm, accounts for6% ofstrokes overall


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Intracerebral Hemorrhage

The most common cause of non-traumaticintracerebral hematoma is hypertensivehemorrhage.

Other causes : amyloid angiopathy, a rupturedvascular malformation, coagulopathy,hemorrhage into a tumor, venous infarction,and drug abuse.


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Thalamichemorrhage(arrow)

extending intothe left lateralventricle

(arrowheads).


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Hypertensive Hemorrhage

Hypertensive hemorrhage accounts for approximately70-90% ofnon-traumatic primary intracerebralhemorrhages. It is commonly due to vasculopathyinvolving deep penetrating arteries of the brain.

Hypertensive hemorrhage has a predilection fordeepstructures including the thalamus, pons,cerebellum, and basal ganglia, particularly theputamen and external capsule. Thus, it often

appears as a high-density hemorrhage in the region ofthe basal ganglia. Blood may extend into theventricular system. Intraventricular extension of thehematoma is associated with a poor prognosis.


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Hypertensivehemorrhage inthe basilganglia.


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Coagulopathy Related Intracerebral

Hemorrhage

Coagulopathy related intracerebral hemorrhagecan be due to drugs such as coumadin or asystemic abnormality such asthrombocytopenia.

On imaging, this hemorrhage often has aheterogeneous appearance due to incompletely

clotted blood. A fluid level within a hematomasuggest coagulopathy as an underlyingmechanism.


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Notice thefluid level

within thehematoma(arrow

H h D t A t i


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Hemorrhage Due to Arteriovenous

Malformation

An underlying arteriovenous malformation(AVM) may or may not be visible on a CT scan.However, prominent vessels adjacent to thehematoma suggest an underlying arteriovenousmalformation. In addition, some arteriovenousmalformations contain dysplastic areas of

calcification and may be visible as serpentineenhancing structures after contrast

administration.


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The CT on the left shows hemorrhage (arrow) due to underlying AVM (arrowheads).The arteriogram on the right shows the tangle of vessels (arrowheads) of the AVM.This lesion would be considered for intravascular embolic therapy.

Subarachnoid Hemorrhage


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Subarachnoid Hemorrhage

In the absence of trauma, the most common cause of

SAH is a ruptured cerebral aneurysm. Cerebralaneurysms tend to occur at branch points ofintracranial vessels and thus are frequently locatedaround the Circle of Willis. Common aneurysm

locations include the anterior and posteriorcommunicating arteries, the middle cerebral arterybifurcation and the tip of the basilar artery.Subarachnoid hemorrhage typically presents as the"worst headache of life" for the patient.

Detection of a subarachnoid hemorrhage is crucialbecause the rehemorrhage rate of rupturedaneurysms is high and rehemorrhage is often fatal.

CT th i i d lit f h i b f it


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CT the imaging modality of choice because of itshigh sensitivity for the detection of subarachnoidhemorrhage. CT is most sensitive for acute

subarachnoid hemorrhage. After a period of days toweeks CT becomes much less sensitive as blood isresorbed from the CSF. If there is a strong clinicalindication, LP may be warranted despite a negative

CT since small bleeds can be unapparent on imaging.On CT, a SAH appears as high density within sulciand cisterns. The insular regions and basilarcisterns should be carefully scrutinized for subtle

signs of subarachnoid hemorrhage. Subarachnoidhemorrhage may have associated intraventricularhemorrhage and hydrocephalus.


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High density bloodfills the cisterns(arrowheads) in

this patient withhemorrhage fromthe left middlecerebral

artery. Note themiddle cerebralartery aneurysm(arrows).

Ischemic stroke


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Ischemic stroke

Ischemic strokes are caused by thrombosis,

embolism of thrombosis, hypoperfusion andlacunar infarctions.

A THROMBOTIC STROKE occurs when a bloodclot within a cerebral artery and blocks or reduces the

flow of blood through the artery. This may be due toan underlying stenosis, rupture of anatherosclerotic plaque, hemorrhage within the wallof the blood vessel, or an underlying hypercoagulable

state. This may be preceded by a TIA

and oftenoccurs at night or in the morning when bloodpressure is low. Thrombotic ischemic strokesaccount for 53% of all strokes.


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HYPOPERFUSION INFARCTION occur under

two circumstances. Global anox

ia may occurfrom cardiac or respiratory failure and presentsan ischemic challenge to the brain. Tissuedownstream from a severe proximal stenosis

of a cerebral artery may undergo a localizedhypoperfusion infarction. Lacunar andhypoperfusion strokes, account for the

remaining 1% of strokes of the ischemic

Imaging of Stroke


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Imaging of Stroke

"Stroke" is a clinical diagnosis; howeverimaging is playing an increasingly importantrole in its diagnosis and management. Themost important issue to determine whenimaging a stroke patient is whether one isdealing with a hemorrhagic or ischemicevent. This has crucial therapeutic and triage

implications.

Decisions that must be made concerning


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Decisions that must be made concerningtherapy are dependent on the diagnosis andmay include the following:- Is the patient a thrombolysis candidate andshould thrombolytic therapy be used?

- Intravenous or intrarterial therapy?

- Neurosurgery or neurology patient?

In addition about 2% of clinically definite

"strokes" are found to be a result of some otherpathology such as a tumor, a subduralhematoma or an infection.

CT scanning


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CT scanning

There are several advantages to performing a CT scan insteadof other imaging modalities. A CT scan:

- Is readily available- Is rapid- Allows easy exclusion of hemorrhage- Allows the assessment of parenchymal damage

The disadvantages of CT include the following:

- Old versus new infarcts is not always clear- No functional information (yet)- Limited evaluation of vertebrobasilar system

A CT is 58% sensitive for infarction within the first 24 hours(Bryan et al, 1991). MRI is 82% sensitive. If the patient isimaged greater than 24 hours after the event, both CT and MRare greater than 90% sensitive.

CT Pathophysiology


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CT Pathophysiology

After a stroke, edema progresses, and braindensity decreases proportionately. Severeischemia results in a 3% increase inintraparenchymal water within 1 hour. Thiscorresponds to 7-8 Hounsfield Unit decreasein brain density. There is also a 6%increase inwater at 6 hours. The degree of edema is

related to the severity of hypoperfusion andthe adequacy of collateral vessels.


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Sharplycircumscribedhypodense

edema(arrowheads)in the rightmiddle cerebral

artery territory.

CT Findings of Stroke


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CT Findings of Stroke

When analyzing the CT of a potential stroke victim,

one of the first findings to look for is the presence orabsence of hemorrhage.

Another common finding in stroke patients is a densemiddle cerebral artery or a dense basilar artery,

which corresponds to thrombus in the affectedvessel.

There are also more subtle changes of acute ischemiadue to edema which include the following:

- Obscuration of the lentiform nuclei- Loss of insular ribbon- Loss of gray/white distinction- Sulcal effacement


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Dense basilarartery (arrow).

Hyperdense Vessel Sign


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Hyperdense Vessel Sign

A hyperdense vessel is defined as a vesseldenser than its counterpart and denser thanany non-calcified vessel of similar size. This isseen in 25% of stroke patients. In patientspresenting with clinical deficit referable to themiddle cerebral artery territory, thehyperdense vessel sign is present 35-50% of

the time. This sign indicates poor outcome andpoor response to IV-TPA therapy.


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Basilar Thrombosis

Thrombosis of the basilar artery is acommon finding in stroke patients. CT

findings include a dense basilar arterywithout contrast injection.


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Dense basilar

artery (arrow).Compare this tothe normalinternal carotid

artery(arrowhead


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Lentiform Nucleus Obscuration

Lentiform nucleus obscuration is due tocytotoxic edema in the basal ganglia.This sign indicates proximal middlecerebral artery occlusion, which resultsin limited flow to lenticulostriate arteries.Lentiform nucleus obscuration can be

seen as early as one hour post onset ofstroke.


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Hypodensity inthe lefthemisphere

(arrows)involving thecaudatenucleus and

lentiform nuclei(globus pallidusand putamen).

Insular Ribbon Sign


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Insular Ribbon Sign

The insular ribbon sign is the loss of the gray-white interface in the lateral margins of the

insula. This area is supplied by the insularsegment of the middle cerebral artery & isparticularly susceptible to ischemia because itis the most distal region from either anterioror posterior collaterals. The insular ribbon

sign may involve only the anterior or theposterior insula.


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The cortex of the left insular ribbon is notvisualized (arrow).

Diffuse Hypodensity and Sulcal Effacement


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Diffuse Hypodensity and Sulcal Effacement

Diffuse hypodensity and sulcal effacement isthe most consistent sign of infarction.Extensive parenchymal hypodensity isassociated with poor outcome. If this sign ispresent in greater than 50% of the middlecerebral artery territory there is, on average, an85% mortality rate. Hypodensity in greater than

one-third of the middle cerebral artery territoryis generally considered to be a contra-indicationto thrombolytic therapy.


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Hypodensityand sulcaleffacement

(arrowheads)in the rightmiddle cerebral

arterydistribution.

CT of Subacute Infarction


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CT of Subacute Infarction

The CT of a subactue infarction has thefollowing findings in 1 -3 days:

- Increasing mass effect- Wedge shaped low density- Hemorrhagic transformation


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After 4 - 7 days the CT is characterized by:- Gyral enhancement

- Persistent mass effect

In 1-8 weeks:

- Mass effect resolves- Enhancement may persist


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This imagewas taken 4hours after

the infarction.


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This image, from the same patient, wastaken 2 days after the infaction.

Enhancement in Infarctions


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Enhancement in Infarctions

90% of infarcts enhance on CT examinationswith IV contrast at 1 week after the infarct.Approximately 35% enhance by 3 days. Faintenhancement begins near the pial surface ornear the infarct margins. The enhancement isinitially smaller than the area of infarction. Itsubsequently becomes gyriform.

Enhancement is due to breakdown of theblood brain barrier, neovascularity, &

reperfusion of damaged brain tissue.


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Post contrast CT scan demonstratinggyriform enhancementof subacute right frontal lobe infarct (arrow

Meningitis


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g

There are three subtypes of meningitis. Acutepyogenic meningitis is usually bacterial.Lymphocytic meningitis is usually viral,benign and self-limited. Chronic meningitis is

often seen in immunocompromised hosts &may be fungal or parasitic.

Imaging in suspected meningitis patients isperformed to look forcomplications and

assess safety of lumbar puncture. Imaging isnot usually performed to diagnose meningitisbecause imaging studies are frequently normaldespite the presence of the disease.


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Hydrocephalus


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y p

Hydrocephalus, a problem with the ratio ofproduction of CSF to its reabsorbtion, is mostfrequent in children.

Communicating hydrocephalus is the mostcommon and is due to arachnoid villi andsubarachnoid space obstruction.

Obstructive hydrocephalus is less common but

may occur as a result of the following:

o Aqueductal stenosis or occlusiono Trapped fourth ventricleo Ependymitis


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In thesesections fromthe same

patient noticethe enlagementof the ventricles

and cisternsthat occurs withhydrocephalus

Ventriculitis / Ependymitis


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p y

Inflammation and enlargement of theventricles characterizes ventriculitis.Ependymitis shows hydrocephalus withdamage to the ependymal lining and

proliferation of subependymal glia.

A CT of patients with these conditions revealsthe presence ofperiventricular edema and

subependymal enhancement. Ventriculitisand Ependymitis affect approximately 30% ofthe adult patients and 90% of the pediatric

patients with meningitis.


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In this post contrastCT scan, note thering enhancing

brain abscess(arrowheads) andenhancement of theependymal lining of

the atrium by the leftlateral ventricle(arrow).

Cerebrovascular Complications of


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Meningitis

The development of cerebrovascular problemsis the most common complication of meningitis.Arterial infarction can occur which often

affects the basal ganglia due to the occlusionof small perforating vessels.

Hemispheric infarction can also occur due to

major vessel spasm. Venous infarctions are also common and can

include cortical venous occlusion or the

involvement of the superior sagittal sinus.

The image on the left shows thrombosis of the superior sagittal sinus (arrow) prior to the


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The image on the left shows thrombosis of the superior sagittal sinus (arrow) prior to the

administration ofcontrast. The image on the right shows the thrombosis in the same patient after contrast

administration.

Extra-axial CNS Infection


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Extra-axial CNS infections can involve epiduralabscess or subdural empyema. Extra-axialCNS infections account for 20-30% of CNSinfections. Fifty percent of extra-axial infections

are associated with sinusitis, usually frontalsinusitis. The infection occurs by directextension or septic thrombophlebitis. 30% ofextra-axial infections occurpost-craniotomy.

Finally, 10-15% of extra-axial CNS infectionsare related to meningitis. CT findings include afocal fluid collection usually with an enhancingmargin in a subdural or epidural location.

Epidural Abscess


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On CT, an epidural abscess appears as a focallow-density epidural mass. Duralenhancement may be present as well. Themass may extend into the subgaleal space. It

also may cross the midline but usually doesnot cross suture lines.


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In the left image notice the rimenhancing epdural fluid

collection (arrowheads). In theright image, notice theopacification of the left frontalsinus due to acute sinusitis(arrow).

Subdural Empyema


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Subdural empyema is usually due to meningitis,sinusitis, trauma or prior surgery. It is aneurosurgical emergency. Subdural empyemaleads to rapid clinical deterioration, especially if

it is due to sinusitis. On CT it appears as anisodense or hypodense extra-axial mass. It

has a lentiform or crescentic shape.

The margin of collection often enhances withcontrast material administration due to thepresence of granulation tissue or subjacent

cortical inflammation.


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Notice theheterogeneous subduralfluidcollection.


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In the samepatient, postcontrastadministration,notice thepatchy

enhancement ofthe fluidcollection

Intracranial Tumors


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Intracranial tumors generally present with afocal neurological deficit, seizure, or headache.


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Multipleenhancingmasses locatedat the grey-whitejunction zones.

Glioblastoma Multiforme


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Glioblastoma Multiforme is the most aggressivegrade of astrocytoma. The two-year survivalrate of patients diagnosed with GlioblastomaMultiforme is 10-15%. On CT, GBM is

characterized by necrosis and irregularenhancement. It is one of very few lesions thatfrequently cross the corpus callosum.


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Notice the ill-defined lowdensity in the

right frontalregion.


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An image postcontrastadministration in

the same patientreveals patchyenhancement, aportion of which is

crossing thecorpus callosum(arrow).

Meningioma


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Meningiomas are the most common extra-axialneoplasm of the brain. Middle-aged women aremost frequently affected. Twenty percent ofmeningiomas calcify. On CT, meningiomas areusually isointense to gray matter.


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Bone windows confirm calcification withinthe mass.


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Axial, postcontrast CTdemonstrati

ng broadbasedenhancing

extra-axialmass.

Alzheimer's Disease - Epidemiology


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Alzheimers disease is a progressive, neurodegenerativedisease that affects >65% of patients with known dementia.

According to the Alzheimers Association, one in ten personsover the age of65 and nearly half of those over age 85 haveAlzheimers disease. Currently, Alzheimer's disease affects 4million Americans and 30 million individuals worldwide with afemale-to-male prevalence of 70%. Within fifty years the

number affected in the U.S. alone is projected to increase to 14million. This population costs the U.S. economy on average$100 billion per year in health care expenditures, and $26billion per year in lost wages. An individual with Alzheimer'sdisease may live an average of 8 years to as many as 20 years

from the initial onset of symptoms. Current treatment includesthe use of acetylcholine esterase inhibitors and most recently aN-methyl-D-aspartate (NMDA) receptor antagonist. However, inmany cases Alzheimer's disease leads to total disability withensuing death secondary to infection, malnutrition, or body

system failure.


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Alzheimer's Disease - Pathophysiology One proposed etiology of Alzheimers disease speculates it results from the

aberrant processing of amyloid precursor protein (APP). This glycoprotein isnormally expressed in high concentrations on neuronal cell surfaces and isexcreted in a soluble form into the extracellular space following cleavage bysecretases. When one of these secretases, beta-secretase, is overlyexpressed, a non-soluble amyloidogenic peptide fragment is generated. It issurmised that this fragment when accumulated extracellularly initiates aninflammatory cascade resulting in oxidative damage and eventual celldeath.

Large cortical neurons in the transentorhinal region are the major types ofneurons that undergo this degeneration. This process begins focally in the

fronto/temporal lobes (primarily the entorhinal cortex and hippocampalregions) succeeded by the parietal lobes and finally the occipital lobes. Theneuronal loss is severe resulting in marked, diffuse atrophy that may be asmuch as 10-30% of the total brain mass.


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Alzheimer's Disease - Imaging Because of its low sensitivity and specificity for the diagnosis of

Alzheimer's disease, imaging is typically not used to rule inAlzheimer's disease but rather to rule out other causes of dementia.Nevertheless, in the right clinical context Alzheimer's disease

appears radiographically as diffuse cerebral atrophy with enlargedlateral ventricles and widened sulci on CT. On thin-section (3 mmthick) coronal T1-weighted MR, medial temporal lobe atrophyprimarily in the amygdala, hippocampus, and parahippocampalgyrus may be visually evident. Utilizing MR volumetricmeasurements, the hippocampal formation may be quantitativelydetermined to show focal atrophy. In addition, the temporal horns,supracellar cisterns, and Sylvian fissures may exhibit focalsymmetric or asymmetric enlargement.


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MR has been chosen for the above images because of its ability to showgreater detail in Alzheimer's disease.The image on the left is a thin-section coronal T1-weighted MRI of an individualwith Alzheimer's.The arrows indicate focal, assymetric atrophy of the right medial temporal lobe.Also visible on the left are the dilated lateral and third ventricles most likely dueto diffuse atrophy.The image on the right is an age-matched control for comparison


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FDG PET reveals temporoparietal metabolicdeficits in patients with Alzheimer's disease.

Although asymmetry is not uncommon, usually

certain brain structures show metabolic sparingincluding the basal ganglia, thalamus,cerebellum, and primary sensorimotor cortex.Finally, on SPECT imaging bilateral

temporoparietal hypoperfusion as well asdecreased uptake in the medial temporal lobesand cingulated regions may be exhibited.


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Both images above are SPECT images using Tc-99 in an individual withsevere Alzheimer's disease.The image on the left is taken as if looking at the patient's lefthemisphere, and vice versa for the image on the right.The arrows indicate bilateral frontal, temporal, and parietalhypoperfusion as seen by areas of hypodensity.

FL = frontal lobe; TL = temporal lobe; PL = parietal lobe


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Parkinson's Disease - Epidemiology Idiopathic Parkinsons disease is a chronic, progressively disabling disease

that falls under the heading of akinetic-rigid syndromes. A clinical syndrome,Parkinson's disease is clinically evident by its triad of bradykinesia andhypokinesia, resting tremor, and increased tonicity of voluntary musculatureand loss of postural reflexes. Parkinsons disease is estimated to affectbetween 500,000 and 1.2 million individuals in the United States. Currently,approximately 50,000 new cases are reported annually. Of those newlydiagnosed with idiopathic Parkinson's disease, 15% are below the age of50. Nationally, 1 in 100 individuals over the age of60 has Parkinson'sdisease with only a slight male predominance. Based on annual direct andindirect costs to society of $25,000 per patient per year, the gross annualeconomic burden to society reaches as high as $25 billion per year. There

is no cure for Parkinson's disease. Current treatment include anticholinergicand dopaminergic medications. If left untreated, Parkinson's diseaseprogresses to frank deterioration of all brain functions and total disability.Consequently, these loss of functions may result in early death


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Parkinson's Disease - Pathophysiology One possible etiology of Parkinson's disease may be a defect in complex 1

of the mitochondrial electron transport chain with resultant dysfunction andproduction of free radicals and oxidative damage. Histopathologically, thereis a selective loss of neuromelanin containing dopaminergic neurons withinthe pars compacta of the substantia nigra. Additionally, the retrorubral areaand ventral tegmental area of the midbrain may also show significantneuronal loss.

Destruction of these neurons leads to disruption of the normal projections tothe neostriatum, limbic structures, and selected cortical forebrain areas.When 80-85% of these nigral neurons degenerate and at least 80% of thestriatal dopamine content is lost, symptoms of this movement disorder may

be manifested. Currently the most commonly employed treatment consistsof dopaminergic and anticholinergic medications.


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Parkinson'sDisease - Imaging Radiographically Parkinsons disease appears as nonspecific

atrophy with enlarged lateral ventricles and widened sulci on CT. OnMR, decreased width of the pars compacta between the parsreticularis and the red nucleus may be evident. Otherwise, no

statistically significant differences in signal intensity or size of thepars compacta have been substantiated.

On PET imaging using 6-fluorodopa (FDOPA), decreased uptake ismost evident in the posterior striatum, particularly in the putamen.

Additionally, PET studies of cerebral glucose metabolism using 18FFluorodeoxyglucose (FDG) show diffuse cortical hypometabolism

most marked in the parietotemporal cortex.


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The two images above are T2-weighted axial images through the midbrain.MR has been chosen in place of CT because of its more specific findings.In the image on the left, the arrows indicate areas of decreased width of the low signalintensity pars compacta within the substantia nigra.This is a subtle but visible finding when comparing to the age-matched control on the right.


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Huntington's Disease - Epidemiology Huntingtons disease is a progressive neurodegenerative disorder

characterized by choreoathetoid movements, behavioraldisturbances, and progressive dementia. Huntington's disease is aknown genetically linked disorder with autosomal dominant

inheritance and complete penetrance. Individuals affected byHuntington's disease are first diagnosed between the ages of 30and 60 and experience a gradual decline in function over a period of10-25 years. Currently there are 30,000 individuals in the U.S. withHuntington's disease and 200,000 individuals at risk of inheriting thedisease. Worldwide 5-10 persons per100,000 people haveHuntington's disease. There is no cure for Huntington's disease.

Current treatment includes dopamine antagonists. Huntington'sdisease is universally fatal. Death is often secondary to infection(most often pneumonia), injuries related to falls, or othercomplications, although suicide is not uncommon.


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Huntington'sDisease - Pathophysiology Huntingtons disease is one of many diseases resulting from an abnormal replication

of a trinucleotide repeat. In the case of Huntington's disease, this trinucleotide repeatis found within the huntingtin gene located on chromosome 4. One postulatedetiology of this disease is that the selective degeneration of medium sized spinyneurons of the striatum may be secondary to the expression of the huntingtin proteinwith its abnormally expanded trinucleotide repeats. These repeats may predisposethe gene to undergo abnormal protein-protein interactions eliciting a novel, altered, orincomplete loss of protein function.

Given that the medium sized spiny neurons comprise roughly 90% of the striatalneurons, their loss severely disrupts critical interneuronal pathways to the globuspallidus and substantia nigra. Eventually corticostriatal pathways are affected as well,including pyramidal projection pathways to the frontal and parietal lobes.

Grossly these changes are initially manifested by striatal atrophy and reduction ofcross-sectional area by 50-60%. Degeneration occurs most prominently in thecaudate tail followed by the body, head, and eventually the putamen and nucleusaccumbens. By the time the disease reaches its terminal phases, 20-30% of the totalbrain mass may be reduced.


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Huntington'sDisease - Imaging Radiographically Huntingtons disease characteristically exhibits caudate atrophy on

imaging. This may be manifested by a decrease in the convexity of the heads of thecaudate bilaterally or by an increase in the relative volume of the lateral ventricles asseen on CT or T1-weighted coronal MR. To a lesser extent putaminal atrophy mayalso be manifested.

One method of referencing the degree of caudate atrophy is to use the ratio betweenintercaudate distance and calvarial width. Known as the bicaudate ratio, the value isfound by measuring the minimum distance between the caudate indentations of thefrontal horns and the distance between the inner tables of the skull along the sameline and multiplying that figure by 100. The Bicaudate Index (BCI) provides a standardby which configured values may be compared to age-matched controls. Thisparameter has been found to correlate well with caudate atrophy.

On T2-weighted MR, increased signal intensity may be found in both caudate andputamen possibly secondary to gliosis, whereas decreased signal intensity in theglobus pallidus and striatum may be related to iron deposition in these structures.FDG PET may only reveal hypometabolism in the caudate nucleus.


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The images above are axial Head CT scans.The image on the left exhibits bilateral caudatehead atrophy (red arrowheads),

as seen by a decrease in the medial convexities,& lateral ventricle dilatation.Generalized atrophy evident as diffuselywidened sulci is also apparent in the image on

the left.The image on the right is an age-matchedcontrol.


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Pick's Disease - Epidemiology Picks Disease is a neurodegenerative disorder that is clinically

evident as behavioral and language disturbances out of proportionto memory deficits. Pick's disease is estimated to be responsible foranywhere between 2-10% of all cases of senile dementia and up to

25% of all cases of presenile dementia. Following Alzheimersdisease and diffuse Lewy body disease, Picks disease is the thirdmost common neurodegenerative cortical dementia. Generally,individuals are affected between the ages of 40 and 65, with nogender predilection. Currently there is no treatment. Pick's diseaseprogresses relatively rapidly with ensuing disability and deathsecondary to infection or body system failure.


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Pick's Disease - Pathophysiology Picks disease is considered in neuropathology as one of the tau-

opathies. Tau is a microtubule-associated protein that is believed toact as a stabilizer of cell structure in neurons. Defects in this proteinin individuals with sporadic (90%) or familial (10%) forms of Picks

disease predispose their cortical neurons to undergo degenerationand vacuolization. These degenerating neurons may also displayPicks bodies, which microscopically are cytoplasmic inclusions thatrepresent ubiquinated tau fibrils. Due to severe neuronal loss andgliosis, atrophy becomes readily apparent in those regions of thecortex most commonly affected, the frontal and temporal lobes. Thisatrophy may be asymmetric.


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The images above are axial Head CT scans.In the image on the left, focal bifrontotemporal atrophy can be seen,as exhibited by marked widening of the frontal and temporal sulci,dilation of the lateral ventricles, and the "knife-like" projections of the gyri.The image on the right is an age-matched control for comparison.


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On nuclear SPECT cerebral perfusion images,one may see hypoperfusion defects in theventromedial frontal region in the frontal variantof Frontotemporal dementia. In the temporal

lobe variant of Frontotemporal dementia, SPECTdemonstrates hypoperfusion in one or bothtemporal lobes and anterolateral temporal lobeatrophy involving the polar region, fusiform,inferolateral gyri with sparing of the hippocampal

formation may be manifested. Invariably the lefttemporal lobe is more affected than the righttemporal lobe.


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Both images above are SPECT images using Tc-99 in an individual with Pick's disease.The image on the left is the individual's left hemisphere, and vice versa on the right.The arrows indicate decreased focal signal intensity in the frontal lobes bilaterally.The remainder of the cortex is spared as is evident by the equal distribution of radiotracer uptake

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