Brain-Neuroradiology Teaching Files

7/30/2019 Brain-Neuroradiology Teaching Files

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Neuroradiology Teaching Files

Department of radiology

Faculty of Medicine

Chiang Mai University

Case 1

20-year-old woman with motorcycle accident

Findings: axial NECT shows biconvex hyperdense extraaxial

mass at left temporal convexity with non-displaced linear

fracture of the overlying temporal bone. The left temporal lobe

is displaced medially with effacement of the ipsilateralsuparsellar cistern. The midbrain is shifted away from the

herniating temporal lobe.

Diagnosis: Skull fracture with left temporal epidural hematoma

(EDH) and left descending transtentorial herniation.

Discussion:• Acute hematoma is high density or high attenuation on CT.

Overlying skull fractures can often be visualized on bone

windows.

• Classic finding of EDH: well-defined biconvex or lentiform-

shaped hyperdense extraaxial mass.

• Associated fracture in 85-95% (with lacerated meningeal artery

or dural sinus)

• 95% supratentorial (most common in the temporal parietal

region)• Classic lucid interval develops in 50% of patient

Frontal EDH

EDH exists in the potential space between the dura andthe inner table of the skull. EDH can cross the midline but

cannot cross cranial sutures where the dura is more firmlyattached.

Extra-axial collections

Case 2

25-year-old man with motorcycle accident

Findings: axial NECT shows crescentic mixed hyper/hypodense

extraaxial mass at the left frontoparietal convexity. The left

cerebral gray-white matter interface is displaced medially. The

lateral ventricles are shifted to the right with mild dilatation of the right lateral ventricle secondary to foramen of Monro

obstruction.

Diagnosis: Left frontoparietal subdural hematoma (SDH) and

subfalcine herniation.

Discussion:• SDH exists between the dura and arachnoid due to stretching

and tearing of bridging cortical veins. SDH can cross sutures

but cannot cross dural attachment.

• Low density areas within the SDH could represent fresh

unclotted blood, serum extruded from the clot, or CSF fromarachnoid tear .

• A definite history of trauma may be lacking, particularly in

elderly patients.

Brain herniation

1.Subfalcine herniation

2.Transtentorial herniation

- Descending (Uncal herniation)

- Ascending

3. Tonsillar herniation

4. External herniation

Brain herniation causes compression of brain, brain stem, nerves, and

blood vessels againts the rigid bony and dural margins

First CT:

Left SDH with left-

to-right subfalcineand left descending

transtentorialherniation

FU CT 4 days

later: left PCA

infarction secondary

to ipsilateral

descendingtranstentorialherniation.

Each examination demonstrates the brain at the time of the study.

No any imaging modality can substitute good clinical history andphysical examination.

Isodense acute EDH Post-op delayed SDH

CT of a head-injured patient whose clinical was notimproved after craniotomy to remove the left EDH.

Case 3

A young man with motorcycle accident

Findings: axial NECT shows multifocal, droplet-shaped, very low

density foci of air within the basal cisterns and right cerebellar fissures (subarachnoid space)

Diagnosis: Traumatic PneumocephalusDiscussion:

• skull base fracture with dural tear and direct communication

with air-containing paranasal sinus or mastoid air cells may

cause pneumocephalus.

• Pneumocephalus can occur in epidural, subdural,subarachnoid space, ventricles or brain parenchyma.

• Most cases of pneumocephalus resolve spontaneously within

• CSF fistulae may occur in the patients presenting with

headache, rhinorrhea and recurrent meningitis. High resolutioncoronal CT, CT cisternography, Isotope tracers and MR

cisternography have been used to localize the fistula site.

Cisternography

shows CSF

Fistula (arrow)

in 2 cases with

posttraumatic CSFrhinorrhea

Case 4

63-year-old patient with hypertension and left hemiparesis

Findings: axial NECT shows a hyperdense mass at right thalamusand deep white matter with extension into the right lateralventricle.

Diagnosis: Acute hypertensive intraparenchymal hemorrhage with

accompanying intraventricular hemorrhage (IVH).Discussion:

• Hypertension is the most common cause of nontraumaticintraparenchymal hemorrhage in elderly patients. Theycommonly occur in the basal ganglia, thalamus, and pons.

• Hemorrhage into the posterior fossa with mass effect or extension into the ventricular system is associated with poor prognosis.

• Vascular malformations (AVM, cavernous angioma) are morecommon causes of hemorrhage in the younger patients.

• Hemorrhagic brain tumors are more complex, heterogenouswith associated edema. They usually has nonhemorrhagicareas that enhance after contrast administration.

• Other causes of nontraumatic intraparenchymal hemorrhageinclude amyloid angiopathy, hemorrhagic transformation of infarction, coagulopathy, venous infarction etc.

Hypertensive hemorrhage

Basal ganglia Thalamus Pons

Criteria for Dx of hypertensive hemorrhage:

1. HT 2. Age > 45 y

3. Common location: BG(60%), thalamus,

pons, cerebellum

Case 5

A patient with sudden onset of headache and alteration of

consciousness

Findings: axial NECT shows diffuse high attenuation or high densitywithin the basal cisterns, Sylvain fissures and cortical sulci. Smallfocal hyperdense hematoma is seen at the left inferior frontallobe. Small amount of hyperdense IVH is also present in occipitalhorns with dilatation of temporal horns from hydrocephalus.

Diagnosis: Diffuse subarachnoid hemorrhage (SAH) with smallintraparenchymal hematoma, small amount of IVH andhydrocephalus.

Discussion:

• SAH exists in CSF space between the arachnoid and pia. SAH

extends into the cisterns and sulci, while SDH does not extendinto the sulci.

• The most common cause of nontraumatic SAH is rupture of intracranial aneurysm. Focal SAH or ICH are helpful in localizingthe bleeding source.

• 90 % of SAH is cleared from the CSF within 1 week. It is difficultto detect SAH on CT if it is a low hematocrit and a delay inscanning. A lumbar puncture revealing red blood cells or xanthochromia may confirm a suspected SAH.

Investigation guideline for patient withsuspected rupture intracranial aneurysm

Plain CT brain

Clinically suspected SAH

CTA and/or DSAor MRA

Repeat DSA 2 weeks

Treatment(+)

SAH (Ruptured ACoA Aneurysm)

NECT DSA

Focal SAH or ICH are helpful in localizing the bleeding source as in thiscase, localized SAH in the anterior interhemispheric fissure due to rupture ACoA aneurysm.

CTA:sagittal MPR

CTA:3D color VR

DSA: lateral view

DSA: frontal view

Aneurysm at the right MCA bifurcation in a 46-year-old woman with sudden headache

and previous CT showed SAH at the suprasellar cistern and the right sylvian fissure.

Case 6

A man presented with right hemiparesis 6 hours PTA

Findings: axial NECT shows a linear hyperdensitywithin the left MCA and hypodensity with loss of G-Wdifferentiation of the left insular cortex and left basal

ganglia.Diagnosis: hyperacute left MCA infarction

Discussion:

• The CT findings in acute cerebral infarction evolvewith time.

• CT scans can detect early signs of MCA infarctionwithin 6 hours in up to 82% of patients.

• Early signs of MCA infarction include a hyperdenseacute intraluminal thrombus in the MCA (hyperdense

MCA sign), obscuration of the lentiform nucleus, andloss of gray-white interface of the insular cortex(insular ribbon sign).

Early sign of MCA Infarct

Hyperdense MCA sign Insular ribbon sign and

obscuration of the lentiform nucleus

Threshold of ischemia

50-60 ml/100 gm/min normal

15-20 ” Neurological

dysfunction

<10 ” infarction

Ischemicpenumbra

CBF in ml/g/min

Regions of decreased CBF can be quantified to three zones:

1. central core with irreversible damage

2. salvageable penumbra (tissue at risk)

3. oligemic penumbra (low flow without risk of cell death)

Stroke onset

Early detection of ischemia

Thrombolytic Rx (iv rtPA)

risk of hemorrhage

(5.2%)

Salvage ischemic brain

Goals of acute stroke imaging “4P”

• Parenchyma: Assess early signs of acute stroke,

R/O hemorrhage or other lesions (tumor, infection)

• Pipes: Assess extra- and intra-cranial circulation for evidence of intravascular thrombus

• Perfusion: Assess CBV, CBF, MTT(TTP)

• Penumbra: Assess tissue at risk of dying if ischemiacontinues without recanalization of intravascular thrombus

Ref: Rowley. AJNR 2001;22:509-601

Acute stroke imaging “4P”

• Parenchyma:

NECT: to exclude hemorrhage, other lesions

large area of infarct(>1/3 of MCA territory)

DWI: detect hyperacute infarction

• Pipes: CTA, MRA

• Perfusion: CTP, MR-PWI

• Penumbra: Perfusion CT (CBV/CBF mismatch)

Perfusion MR (Diffusion/perfusion mismatch)

Patients with ischemic stroke who could be treated with rtPA

• Onset of symptoms < 3 hours before Rx

• No head trauma or prior stroke in previous 3 months

• No myocardial infarction in previous 3 months

• No GI or urinary tract hemorrhage in previous 21 days

• No major surgery in the previous 14 days

• No history of previous intracranial hemorrhage

• BP: systolic <185, diastolic < 110

• No seizure with postictal residual neurological

impairment….

Ref: AHA/ASA Scientific statement.

Acute stroke imaging protocol

Stroke fast track

Plain CT brain within 3 hours

Indication for thrombolytic Rx (IV rt-PA)

Normal CT or early sign infarction

Contraindication to thrombolytic Rx:

hemorrhage

large area of infarct (>1/3 of MCA territory)

Acute MCA infarction

78 –year-old woman with sudden left hemiparesis 1 day PTA

NECT shows a hypodense area of large infarction involving

the right middle cerebral artery vascular territory.

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