Category Archives: NEURO

STROKE IMAGING

STROKE IMAGING IS EASY TO UNDERSTAND , YET VERY IMPORTANT TO EVERY DOCTOR

Stroke :

 A term that describes an acute episode of neurologic deficit.
 80% of strokes are due to cerebral ischemia (embolic or thrombotic).
 Transient ischemic attacks (TIAs) are focal neurologic events that resolve within 24 hours.
 Those that resolve after 24 hours are called reversible ischemic neurologic deficits (RINDs).

Causes:

1) Cerebral infarction, 80%: o   Atherosclerosis-related occlusion of vessels, 60%

o   Cardiac emboli, 15%

o   Other, 5%

2) Intracranial hemorrhage, 15%
3) Non-traumatic SAH, 5%
4) Venous occlusion, 1%

 

  • Atherosclerotic disease:
  • Atherosclerosis represents the most common cause of cerebral ischemia/infarction.
  • Carotid atherosclerosis causes embolic ischemia;
  • Intracranial atherosclerosis causes in-situ thrombotic or distal embolic ischemia.
  • Location:
  • ICA origin > distal basilar > carotid siphon, MCA.
  • Critical carotid stenosis:
  • Defined as a stenosis of >70% in luminal diameter.
  • Patients with critical stenosis & symptoms have an é risk of stroke & benefit from carotid endarterectomy.
  • Patients with stenosis < 70% or who are asymptomatic are usually treated medically.
  • Imaging Features:
Gray-scale imaging (B-scan) of carotid arteries: o   Evaluate plaque morphology/extent

o   Determine severity of stenosis (residual lumen)

o   Other features:

§  Slim sign à collapse of ICA above stenosis

§  Collateral circulation

Doppler imaging of carotid arteries:

 

o   Severity of stenosis determined by measuring peak systolic velocity:

§  50 70% à velocity 125 to 250 cm/sec

§  70 90% à velocity 250 to 400 cm/sec

§  > 90% à velocity >400 cm/sec

o   Stenoses > 95% may result in decreased velocity (<25 cm/sec)

o   90% accuracy for >50% stenoses

o   Other measures used for quantifying stenosis:

§  End diastolic velocity (severe stenosis à >100 cm/sec)

§  ICA/CCA peak systolic velocity ratio (severe stenosis à >4)

§  ICA/CCA peak end-diastolic velocity ratio

o   Innominate artery stenosis may cause right CCA/ICA parvus tardus

o   CCA occlusion may result in reversal of flow in ECA

Color Doppler flow imaging of carotid arteries: o   High-grade stenosis with minimal flow (string sign in angiography) is detected more reliably than with conventional Doppler US.
CT and MR angiography Are used for confirmation of US diagnosis of carotid stenosis:

o   On CTA, 1.0- to 1.5-mm residual lumen corresponds to 70%-90% stenosis.

o   To determine complete occlusion versus a string sign (near but not complete occlusion), delayed images must be obtained immediately after the initial contrast images.

o   At some institutions, carotid endarterectomy is performed on the basis of US and CTA/MRA if the results are concordant.

o   Pitfalls of US and MRA in the diagnosis of carotid stenosis:

§  Near occlusions (may be over diagnosed as occluded)

§  Post-endarterectomy (complex flow, clip artifacts)

§  Ulcerated plaques (suboptimal detection)

§  Tandem lesions (easily missed)

Carotid arteriography: The gold standard is primarily used for:

o   Post-endarterectomy patient

o   Accurate evaluation of tandem lesions and collateral circulation

o   Evaluation of aortic arch and great vessels

o   Discordant MRA/CTA & US results

  • Cerebral ischemia & infarction:
  • Cerebral ischemia:
  • Refers to a diminished blood supply to the brain.
  • Infarction:
  • Refers to brain damage, being the result of ischemia.
  • Causes:
Large vessel occlusion, 50%
Small vessel occlusion (lacunar infarcts), 20%
Emboli: o   Cardiac, 15%:

§  Arrhythmia, atrial fibrillation

§  Endocarditis

§  Atrial myxoma

§  MI (anterior infarction)

§  Left ventricular aneurysm

o   Non-cardiac:

§  Atherosclerosis

§  Fat, air embolism

Vasculitis: o   SLE

o   Polyarteritis nodosa

Other:

 

 

 

 

 

 

 

o   Hypo-perfusion (border-zone or watershed infarcts)

o   Vasospasm: ruptured aneurysm, SAH

o   Hematologic abnormalities:

§  Hypercoagulable states

§  Hb abnormalities (CO poisoning, sickle cell)

o   Venous occlusion

o   Moyamoya disease

  • Imaging Features:
Angiographic signs of cerebral infarction: o   Vessel occlusion, 50%

o   Slow antegrade flow, delayed arterial emptying, 15%

o   Collateral filling, 20%

o   Non-perfused areas, 5%

o   Vascular blush (luxury perfusion), 20%

o   AV shunting, 10%

o   Mass effect, 40%

Cross-sectional imaging: Ø CT à the 1.st study of choice in acute stroke in order to exclude:

ü Intracranial hemorrhage.

ü Underlying mass/AVM.

Ø Most CT examinations are normal in early stroke.

Ø Early CT signs of cerebral infarction include:

·        Loss of gray-white interfaces (insular ribbon sign)

·        Sulcal effacement

·        Hyper-dense clot in artery on NCCT (dense MCA sign)

Ø Edema (maximum edema occurs 3 5 days after infarction):

§  Cytotoxic edema àdevelops within 6 hours (detectable by MRI).

§  Vasogenic edema àdevelops later (first detectable by CT at 12 24 hours).

Ø Characteristic differences () distributions of infarcts:

§  Embolic à periphery, wedge shaped

§  Hypo-perfusion in watershed areas of ACA/ MCA and MCA/PCA

§  Border-zone infarcts

§  Basal ganglia infarcts

§  Generalized cortical laminar necrosis

Ø Reperfusion hemorrhage is not uncommon after 48 hours:

§  MRI much more sensitive than CT in detection

§  Most hemorrhages are petechial or gyral.

Ø Mass effect in acute infarction:

ü Sulcal effacement

ü Ventricular compression

Ø Sub-acute infarcts:

ü Hemorrhagic component, 40%

ü Gyral or patchy contrast enhancement (1 3 weeks)

ü GWM edema

Ø Chronic infarcts:

ü Focal tissue loss à atrophy, porencephaly, cavitation, focal ventricular dilatation

ü Wallerian degeneration à distal axonal breakdown along white-matter tracks

 

CT & MRI appearances of infarcts:

Factor 1st Day 1st Week 1st Month > 1 Month
Stage: Acute Early subacute Late subacute Chronic
CT density:  Subtle decrease Decrease Hypodense Hypodense
MRI: T2W: edema T2W: edema Varied T1W dark, T2W bright
Mass effect: Mild Maximum Resolving Encephalomalacia
Hemorrhage: No Most likely here Variable MRI detectable
Enhancement: No Yes; maximum at 2-3 weeks Decreasing No
  • Pearls:
  • Cerebral infarcts cannot be excluded on the basis of a negative CT.
  • MRI with diffusion weighted imaging (DWI) & perfusion weighted imaging (PWI) should be performed immediately if an acute infarct is suspected.
  • CM administration is àreserved for clinical problem cases & should not be routinely given, particularly on the first examination.
  • Luxury perfusion refers to hyperemia of an ischemic area:
  • The increased blood flow is thought to be due to compensatory vasodilatation 2.ry to parenchymal lactic acidosis.
  • Cerebral infarcts have à a peripheral rim of viable but ischemic tissue (penumbra).
§  Acute cerebral ischemia may result in a central irreversibly infarcted tissue core surrounded by peripheral region of stunned cells that is called àa penumbra

§  These cells have ceased to function, but this region is potentially salvageable with early re-canalization.

  • Thrombotic & embolic infarcts occur in vascular distributions àe., MCA, ACA, PCA, etc.
  • MR perfusion/diffusion studies are àimaging studies of choice in acute stroke:
  • DWI detects reduced diffusion coefficient in acute infarction, which is thought to reflect cytotoxic edema.
  • In patients with multiple T2W signal abnormalities from a variety of causes, DWI can identify those signal abnormalities that arise from acute infarction.
  • 50% of patients with TIA have DWI abnormality.
  • MRI in acute stroke:
  • On PD/T2WI and FLAIR infarction is seen as àhigh
  • These sequences detect 80% of infarctions before à24 hours.
  • They may be negative up to à2 4hours post-ictus!
  • High signal on conventional MR-sequences is comparable to àhypo-density on CT.
  • It is the result of irreversible injury with cell death.
  • So hyper-intensity means BAD news à dead brain.
Hyper-intensity on MR = irreversible ischemic brain damage
  • Comprehensive Stroke Protocol: MR
MRI: o   Sag T1, Ax T2, Ax DWI
MRA: o   TOF head & neck
MRA: o   elliptic-centric arch /carotids
Perfusion: ü Single dose Gad

ü GRE-EPI

ü Automated arterial input function

ü Parameter maps: CBV, MTT, CBF

 

Post Gad: o   ax T1, coronal T2 FLAIR
  • Imaging features:
Loss of flow voids: o   Artery or vein.
Loss of Flow-Related Enhancement
Intravascular enhancement: o   DD of intra-vscular enhancement:

ü Meningitis

ü Sturge-Weber syndrome

ü Sarcoid

ü Tumor

Parenchymal Enhancement: o   Rule of 3’s à starts 3days, peaks 3 weeks, gone 3 months.

o   Parenchymal MR Imaging in Stroke:

ü Confirm diagnosis

ü Ischemic vs. hemorrhagic

ü Underlying cause

ü Risk of progression:

v Location

v Size

v Complications

ü Mass effect / herniation

ü Hemorrhagic transformation

Pearl:

  • MRI is better than CT for Hemorrhage:
  • MRI may be as accurate as CT for the detection of acute hemorrhage in patients presenting with acute focal stroke symptoms.
  • MRI is more accurate than CT for the detection of chronic intra-cerebral hemorrhage.
  • Diffusion & perfusion imaging in stroke:
  • Standard diffusion protocol includes a DWI & an apparent diffusion coefficient (ADC) image àusually interpreted side by side:
DWI: o   Summation of diffusion + T2 effects.

o   Abnormalities appear as à high signal.

ADC: o   Diffusion effects only.

o   Abnormalities appear as àlow signal.

Perfusion imaging:

  • Performed using the susceptibility effects of a rapid bolus injection of gadolinium administered intravenously.
  • Rapid continuous scanning during this injection allows the signal changes associated with the gadolinium to be plotted over time for a selected brain volume.
  • These time-signal plots can be processed to yield several possible parameters relating to cerebral perfusion.

 

  • Vascular (perfusion) parameters:
Mean Transit Time: (MTT) §  Measured in àseconds.

§  A measure of how long it takes blood to reach the particular region of the brain.

Cerebral Blood Volume: (CBV) §  Measured in àrelative units &

§  Correlates to the total volume of circulating blood in the voxel.

Cerebral Blood Flow: (CBF) §  Measured in àrelative units &

§  Correlates to the flow of blood in the voxel.

 

 

  • Interpretation:
  • Stroke Evolution on MRI: 
Sequence Hyper-acute

(< 6hours)

Acute

(> 6 hours)

Sub-acute

(Days to weeks)

Chronic
DWI High High High (ê with time) Iso-intense to bright
ADC Low Low Low to iso-intense Iso-intense to bright
TW2/Flair Iso-intense Slightly bright to bright Bright Bright
  • A typical infarct is DWI bright & ADC dark.
  • Gliosis appears DWI bright due to T2 shine-through but is also bright on ADC.
  • DWI:
  • Very sensitive for detecting disease àwill pick up infarcts from about 30 minutes onward.
  • But is non-specific & will also detect non-ischemic disease.
  • ADC:
  • Less sensitive than DWI.
  • But dark signal is fairly specific for restricted diffusion, which usually means ischemia.
  • Significance of a DWI-bright, ADC-dark lesion:
  • This tissue will almost certainly go on to infarct & full necrosis.
  • Rare instances of reversible lesions have been reported àvenous thrombosis, seizures, hemiplegic migraine and hyper-acute arterial thrombosis.
  • Match and mismatch:
  • In the acute stroke setting, a region that shows àmatched both diffusion and perfusion abnormalities is thought to represent irreversibly infarcted tissue,
  • While a region that shows àmismatched perfusion abnormalities and diffusion likely represents viable ischemic tissue, or a penumbra
EXP: (exponential) o   The map that “subtracts” the T2 effect.

o   In equivocal cases, use EXP map as àa problem solver:

ü If it stays bright on the EXP map, then it is àtrue restricted diffusion.

MTT: o   Highly sensitive for disturbances in perfusion.

o   But not good for prediction of later events.

ü For example à an asymptomatic carotid occlusion would have a dramatically abnormal MTT, without the patient being distressed.

CBV: o   A parameter that changes late in the ischemic cascade, &

o   Usually reduced CBV is also accompanied by restricted diffusion..

o   Reduced CBV + restricted diffusion àcorrelate well with tissue that goes on to infarction.

CBF: o   In experimental setting:

ü Can be used to predict the likelihood of brain tissue infarcting.

o   In current clinical practice:

ü If a CBF abnormality exceeding the DWI abnormality (diffusion- perfusion mismatch):

§  This implies that there is brain at risk that has not infracted yet.

§  This brain at risk is the target of therapeutic interventions.

Role of CT/CTA in acute stroke:

Value:

1)    Important in early stages of stroke evaluation to facilitate thrombolytic therapy.

2)    CTA:

§  Demonstrates the anatomic details of the neuro-vasculature from the great vessel origins at the aortic arch to their intracranial termination.

§  Highly accurate in the identification of proximal large vessel circle of Willis occlusions &

§  Therefore in the rapid triage of patients to intra-arterial (IA) or intravenous (IV) thrombolytic therapy.

 

 

CT Early signs of ischemia:

Hypo attenuating brain tissue: o   The reason we see ischemia on CT is that in ischemia cytotoxic edema develops as a result of failure of the ion-pumps.

o   These fail due to an inadequate supply of ATP.

o   An increase of brain water content by 1% will result in a CT attenuation decrease of 2.5 HU.

o   Hypo-attenuation on CT is highly specific for irreversible ischemic brain damage if it is detected within first 6 hours.

o   Patients who present with symptoms of stroke and who demonstrate hypo-density on CT within first 6 hours were proven to have larger infarct volumes, more severe symptoms, less favorable clinical courses and they even have a higher risk of hemorrhage.

o   Therefore whenever you see hypo-density in a patient with stroke this means bad news.

o   No hypodensity on CT is a good sign.

Hypo-density on CT = irreversible ischemic brain damage
Obscuration of the lentiform nucleus: o   Obscuration of the lentiform nucleus, also called blurred basal ganglia, is an important sign of infarction.

o   It is seen in MCA infarction & is one of the earliest & most frequently seen signs.

o   The basal ganglia are almost always involved in MCA infarction.

Insular Ribbon sign: o   This refers to hypo-density & swelling of insular cortex.

o   It is a very indicative & subtle early CT-sign of infarction in the territory of MCA.

o   This region is very sensitive to ischemia because it is the furthest removed from collateral flow.

o   It has to be differentiated from herpes encephalitis.

Dense MCA sign: o   This is a result of thrombus or embolus in the MCA.

o   On CT-angiography occlusion of the MCA is visible.

Loss of sulcal effacement
  • Technique:
  • Stroke protocol (CT/CTP/CTA):
NCCT:

(done first)

§  Value:

o   To exclude hemorrhage àan absolute contraindication to thrombolytic therapy.

o   To detect irreversible “core” of infarction (>1⁄3 of a vascular territory) à a relative contraindication to thrombolysis.

§  Scanning parameters:

o   140 kV, 170 mA, pitch = “high quality” (3: 1)

o   Table speed à 7.5 mm/sec.

o   Scanning from à skull base to vertex.

o   Slice thickness à 5 mm

o   Window width ànarrow settings, with a center level of about 30 HU (width of 5 to 30 HU):

v This facilitates the detection of early, subtle, ischemic changes contiguous with normal parenchyma.

CTP: §  Scanning parameters:

o   IV contrast bolus ~ 50 cc

o   Dynamic scanning ~ 45 seconds

o   4-8 slices

o   5 mm

o   Calculate perfusion parameters:

v Cerebral blood volume CBV

v Mean transit time MTT

v Cerebral blood flow CBF

CTA: §  Scanning parameters:

Initial phase scan parameters:

o   IV contrast (non-ionic, non-osmolar CM) bolus 100 ml (90-120 ml) à   4 cc/sec

o   Scan delay of à 25 sec.

v A longer delay may be needed for patients with à compromised cardiac function & atrial fibrillation.

o   Scanning from à skull base to the vertex

o   Used parameters are as per the NCCT scan.

Second phase scan parameters:

o   Performed immediately after initial scan, with minimal possible delay.

o   Scanning from the aortic arch to the skull base.

o   Similar scan parameters except for àan é in the table speed to 15 mm/sec.

§  Note that:

o   Major advantages of first scanning the intracranial circulation include:

v obtaining the most important data first, which can be reviewed during subsequent acquisition;

v allowing time for clearance of dense IV contrast from the subclavian, axillary, and other veins at the thoracic inlet, reducing streak artifact

o   On a >16-slice scanner, CTA may be performed from the vertex to the aortic arch in one pass,

v This gets rid of the loss of contrast enhancement in the neck CTA usually seen with a two-stack protocol

  • Lacunar infarcts:
  • Lacunar infarcts:
  • Account for à20% of all strokes.
  • The term refers to à occlusion of penetrating cerebral arterioles
  • Commonly affected are:
§  Thalamoperforators (thalamus)

§  Lenticulostriates (caudate, putamen, internal capsule)

§  Brainstem perforator (pons)

  • Usually cause characteristic clinical syndromes:
  • Pure motor hemiparesis, pure hemisensory deficit, hemiparetic ataxia, or dysarthria-hand deficit.
  • Imaging Features:
o   MRI is àthe imaging study of choice.

o   Small ovoid lesion (< 1 cm):

§  Hyper-intense on T2W & proton density–weighted (PDW) image.

o   Location of lesions is very helpful in DDx:

ü Dilated peri-vascular or Virchow-Robin (VR) space:

§  Can be large (giant VR space), can cause mass effect & can have surrounding gliosis

§  More elongated appearance on coronal images

Therapeutic options:

  • Within 3 hours of stroke onset à IV thrombolysis + recombinant tissue plasminogen activator (r-tPA)
  • If > 3 hours of stroke onset à no IV thrombolysis given (é probability of intracranial hemorrhage)
  • The time window for treatment with IA agents is:
  • Twice as long for the anterior circulation &
  • Indefinite for the posterior circulation.
  • For thrombosis localized to the posterior circulation:
  • The time window for treatment may be extended beyond 6 hours due to the extreme consequences of loss of blood flow to the brainstem, despite the risk of hemorrhage.
  • Advanced CTA/CTP imaging of acute stroke:
  • Has the potential to not only help exclude patients at high risk for hemorrhage from thrombolysis,
  • But also identify those patients most likely to benefit from thrombolysis.
  • Even without hemorrhage, treatment failure with thrombolytics is not uncommon.
  • The choice between IA & IV thrombolysis depends on a variety of factors, including:
o   the time post ictus,

o   the clinical status of the patient, &

o   whether the clot is proximal (IA) or distal (IV).

  • When typical findings of occlusive thrombus on CTA & ê tissue enhancement on CTP are not present, the DDx include:
o   Lacunar infarct.

o   Early small distal embolic infarct.

o   Transient ischemic attack.

o   Complex migraine headaches.

o   Seizure.

  • Golden points:
What you like to know? §  Is there hemorrhage?

§  How extensive is the edema?

Answer à CT
§  Where’s the occlusion?

§  What’s the blood flow?

§  How much brain is dead?

§  How much brain is at risk?

Answer à MRA-PWI-DWI- CT- CTA-CTP
4 P: o   PARENCHYMA:

§  Exclude Hge.

§  Early signs of stroke.

o   PIPES

§  Intra-cranial circulation.

§  Extra-cranial  circulation

o   PERFUSION à CBV –CBF –MTT

o   PENUMBRA       : Tissue at risk of dying

 

MRI GLIOBLASTOMA MULTIFORM (GBM MRI)

GBM MRI

This is a well known medical truth that Glioblastoma is the most malignant tumor of the brain. It has different terms, it may be called Grade IV astrocytoma or malignant astrocytoma or glioblastoma multiforme (GBM), Here we will discuss MRI Glioblastoma.

Glioblastoma In another word is a fast growing malignant astrocytic tumor which has special characters of having necrosis and neovascularity. considering 1ry malignant intracranial neoplasm, GBM is the most common tumor.

Glioblastoma has 2 types: the first type is Primary or could be named de novo. The second type is secondary, as degeneration
from astrocytoma that has a lower grade, and characterized by necrosis and microvascular proliferation.

According to WHO classifications. According to WHO grading, GBM is grade IV (1).

GBM is which is the most malignant astrocytic tumor, makes about 15% to 20% of all intracranial tumors. In adults, GBM is considered the most wide-spreading primary brain neoplasm (2).

It is believed that most glioblastomas arise from an existent astrocytoma or anaplastic astrocytoma, but few could grow as the primary tumor. According to a clinicopathologic study of 241 gliomas with necropsy data, about 7.5% of glioblastomas appear to have a multicentric origin(3).

Age incidence of GBM is markedly increased after the age of 50. its peak incidence appears more prominent in the sixth decade. GBM is very rare to occur in young age especially less than 30 years.Male to Female ratio is 3:2, it has male prominence as all type of glioma.

The same occurs in clinical presentation, a symptom of rapid increase intracranial pressure, after a short period of one month from its beginning. These forms of tumors have the worst prognosis with the median survival of 12 months.

Good prognosis cause includes young age, GBM occurring as a secondary to another lesion, not as a primary tumor, the third one is surgical debulking (4).

 

Pathological Process and clinical presentation of  GBM 


          GBM pathological malignant characters are a reflection in the MR imaging, and unfortunately, MR imaging suffers from som

e of the limitations seen on pathologic examination.

At the MR, we could see the heterogenicity inside the tumors which is the image of the necrosis and hemorrhage and hypercellularity (5). T2-WI would be very helpful to detect these changes, in this sequence cystic necrosis foci and hemorrhage is shown with debris–fluid levels and lower-intensity regions in areas of hypercellularity.

on spin echo, MR imaging, within the tumors linear regions of the signal void are seen, which reflect the effect of angiogenesis that characterizes glioblastomas. it’s very rare to find calcification in these lesions except they arise in lesions which have a low grade.

The bleeding tumor is a character of GBM, but unfortunately not alone, other tumors as oligodendroglioma and ependymoma have this character, so In MR we should be aware to the good differentiation between Intratumoral hemorrhage and Benign hemorrhage this is well described in the table below (Table 1).

The extensive edema (appear more prominent on WM) associated with this tumor makes a significant mass effect. So it’s very important to define tumor margins and differentiate it from surrounding edema.In the real world, what we call edema is very precise to be described as “tumor plus edema“(6).

The is appears on MR imaging more clear than CT, especially with the improvement of the MR contrast resolution imaging. So every radiologist and physician should know that tumor extends beyond the appeared abnormality regions MRI (7).

Patient with glioblastoma Symptoms usually varies with location. They may present with Seizures, focal neurologic deficits which are common to affect a motor area or limb function. Age Peak of glioblastoma range from 45 to 75 years, although it’s rare in young patients it may occur at any age.gliobasltoma has Relentless progression, its survival rate often < 1 year (8).

Intratumoral hemorrhage Benign hemorrhage
Markedly heterogeneous, related to
Mixed stages of blood
Debris–fluid (intracellular–extracellular blood) levels
Edema + tumor + necrosis with blood
Shows expected signal intensities of acute, subacute, or chronic blood, depending on stage of hematoma
Identification of nonhemorrhagic tumor component No abnormal nonhemorrhagic mass
Delayed evolution of blood-breakdown products Follows expected orderly progression
Absent, diminished, or irregular ferritin/hemosiderin Regular complete ferritin/hemosiderin rim
Persistent surrounding high intensity on long–repetition time images (i.e., tumor/edema) and mass effect, even in late stages Complete resolution of edema and mass effect in chronic stages

Table (1): Difference between Mlaginent intratumoral Hge Vs Bening intracranial Hematoma.(9) (Table 11.8)

Figure (1): Glioblastoma multiforme, gross specimen. A brain section from an autopsy specimen shows a nonhomogeneous cut surface with hemorrhage and necrosis. (Courtesy of Dr. N. K. Gonatas, Pennsylvania University Hospital, Philadelphia, Pennsylvania. (10)

MRI sequences of Localize and characterizations of GBM.

MRI is the best imaging choice for localization and characterization of Glioblastoma. Contrast-enhanced MR is most sensitive, Newer techniques help improve diagnosis/biopsy accuracy like MRS, perfusion, hypoxia imaging, DTI.

Glioblastoma appears as thick, irregularly enhancing tumor, has a  necrotic core.The mass could be seen as heterogeneous, hyperintense mass associated with adjacent infiltration of the tumor and vasogenic edema. (11)

With GBM we could expect to see necrosis, hemorrhage, cysts, fluid levels, neovascularity. GBM may appear diffuse infiltrative mass, and appear necrotic and have poor margins, GBM could cross WM and affect the other side of the cerebral hemisphere, If it occurs and affects corpus callosum, it’s so called butterfly tumor.it may include also anterior and posterior commissures. It’s rare to invade meninges and rarely to be multifocal (~5%).(12)

Most common Location of GBM is supratentorial white matter (WM), the frontal, temporal, parietal which are more likely to be invaded by GBM more than occipital lobes.Cerebral hemispheres are more likely than brainstem, which is more probable location than cerebellum.

Basal ganglia and thalamus are less common(13). In children, brain stem and cerebellum are more common. (14)

So, let’s talk a look at MRI sequences used to help localization and characterization of glioblastoma multiform, and how it appears in each sequence.

T1 Weighted Image: GBM appears as irregular isointense, hypointense WM mass. It’s common to see irregular margins and cyst and of course, necrosis is the main sign. Also, GBM could cause subacute hemorrhage.(15)

T2 Weighted Image: GBM appears as heterogeneous, hyper intense mass with adjacent tumor infiltration or vasogenic edema. We expect to see expect to see hemorrhage,  necrosis, cysts, fluid levels, neovascularity. Viable tumor extends far beyond signal changes. (16)

FLAIR: GBM appears as heterogeneous, hyper intense tumor, associated with infiltration and vasogenic edema. (17)

GRE T2-Weighted MRI: there is the probability of artifact that related to products of the blood. (18)

PWI: in this sequence elevated maximum relative cerebral blood volume in comparison with low-grade tumors, also it has elevated permeability in comparison to low-grade tumors. (19)

T1WI C+: on the sequence, the tumor appears as an irregular enhanced tumor with central necrosis .the tumor enhancement could be patchy or nodular or ring shape. (20)

Figure (2): T1-WI GBM appears as hypo intense lesion affecting corpus callosum genu  forming what is called a butterfly tumor (21)

 

 

Figure (3): T2-WI, GBM appears as hyper intense lesion affecting corpus callosum genu  forming what is called a butterfly tumor (22)

 

Figure (4): (GBM MRI) Axial T1WI C+ FS MR in a 60-year-old man with acute onset of seizures shows a heterogeneously enhancing occipital lobe mass with central necrosis and extension across the splenium of the corpus callosum , characteristic of GBM. The frontal and temporal lobes are the most common locations for GBM.(23)

 

 

Figure (5): (GBM MRI)Axial T1 C+ FS MR in the same patient shows a thick enhancing rind of tumor that surrounds the necrotic tumor core, characteristic of GBM. Other lesions including lymphoma and demyelination may also involve the corpus callosum.(24)

Figure (6):(GBM MRI) Axial FLAIR MR in a patient with GBM shows a heterogeneous mass and the typical extensive surrounding signal abnormality that represents a combination of tumor cells and vasogenic edema. Pathologically, tumor cells are found beyond the regions of signal abnormality.(25)

Figure (7):(GBM MRI) MRS in a patient with recurrent GBM shows a classic malignant tumor spectrum with a markedly elevated choline (Cho) , a low NAA at 2.02 ppm, and an inverted lactate peak  at 1.33. (26)

Sequences are used to plan treatment, assess the completeness of treatment and detect a change in the lesion.

DWI is the best MRI used to accurate pre-operative diagnosis, and also to monitor treatment effects on lesion and differentiation between true and pseudo progression. As Glioblastoma has Lower measured ADC than low-grade gliomas, and there is variable diffusion restriction in solid portions of the tumor.(27)

Figure (8): Axial MR perfusion in the same patient shows an increased rCBV . in the solid parts of the tumor and a low rCBV in the necrotic center .Perfusion MR is helpful to provide an accurate preoperative diagnosis. In addition, it is often used to help guide a biopsy if the location of the tumor prevents the patient from undergoing a complete resection.(28)

 

 

As ADC maps present a very good service to assess tumor grading and effect of treatment. Histogram analysis based on ADC  maps of contrast enhanced Tumor provide a great assessment True from pseudo progression.

Yet we should also assess biomarkers values, e.x percentile values of cumulative ADC histogram . to the good differentiation between true and pseudo progression of the tumor, we should know that at Histogram, the underlying hypothesis indicates the viable tumor components while the higher one indicates the edema and necrotic tissue. this sequence is very useful with heterogeneous nature of glioblastomas that include mixed parts of the active tumor and necrotic parts.(29)

DWI is useful not just in that, it’s also very helpful to differentiate between radiation affection and tumor recurrence and progression by assessment of ADC value differentiate of the GBM during after therapy examinations. (30)

Figure (9): This sequences of MR images of the patient on therapy. These represent the phenomenon of pseudoprogression. Note the upper images were obtained just after initiation of treatment show restriction of enhancement which indicates regression of tumor while the tumor is still growing as illustrated in lower images. Lower images were obtained 1 month later show the enlarged tumor.(31)

 

Diffusion tensor imaging (DTI): can also be used to improve surgical planning.(32)

Perfusion Weighted Imaging (PWI): this sequence is more accurate in illustration tumor outlines, so is very helpful in radiation and surgical planning.also, it’s helpful in the assessment of patients response to radiotherapy by measuring of rCBV. (33)

Functional MRI:  it’s the sequence used to the good planning of the neurological risks and treatment of the tumors. As fMRI helps in localization of the invasion of the cortical center that is responsible for the vital functions like memory, motor, and language .it can alter a neurosurgical decision to approach the GBM either by surgery or not.(34)

MRI Sequences used to grade GBM condition.

In addition to previously described routine anatomical sequences ( T1W C+ and T2W, etc). theses sequence are helpful in the grading of Glioblastoma.

MR perfusion very clever in assessment of tumor components that have a higher grade especially in guiding stereotactic biopsy and provide a good estimation of grading of tumors.(35)

Figure (10): An Example of MR perfusion of (GBM) (36)

Spectroscopy:
it’s used in combination with MRI, MRS to evaluate Glioblastoma type and grade, as the high-grade GBM has higher Cho/Cr and Cho/NAA ratios and also have lipid and lactate as result of necrosis
(Figure 6). it’s  used to differentiate the tumor when it enhances from other enhancement cause (e.g necrosis ), also it’s used to  differentiating the tumor when it does not enhance from edema and other T2 prolongation causes.(37)

Figure (11): An Example of Spectroscopy of (GBM) (38)

 

Functional MRI
Functional MRI is very helpful in grading the condition of glioblastoma patient condition . as it used to map language function. Language paradigms vary with  Tumor location. Yet till now  no a dependable way to measure memory tasks for neurosurgical planning.  fMRI used also for Motor mapping depending on the location of the tumor.(39)

Figure (12): Example of fMRI image of Glioblastoma (40)

Generally speaking, the integration of several techniques of advanced imaging (such as spectroscopy, perfusion imaging, and functional MRI) is very helpful in grading good assessment of the pathological process of glioblastoma.

 

 

 

Treatment options and outcomes for the patient

The usual course of treatment of glioblastoma include Biopsy, then tumor debulking followed by XRT, chemotherapy (temozolomide). Newer anti-angiogenesis agents, particularly bevacizumab (vascular endothelial growth factor blocker) for recurrent disease, let’s talk about it :

 

Radiation therapy: Studies show that radiation therapy, when combined with surgery, give prolonged survival rate if we compared it to the choice of surgery alone. It increases survival from three to four months to seven to twelve months.(41)

 

Chemotherapy – Antineoplastic agents:  No optimal chemotherapeutic regimen could be defined till now, however many studies say that about more than 25% of patient receive adjuvant chemotherapy have a more prolonged survival benefits.(42)

 

Surgery: Many studies say that surgery (biopsy vs resection) have a very important effect on survival length . in a study proves that high-grade GBM who underwent total resection, get two years survival incidence up to 19%.(43) .

in another patient, when we do a subtotal resection, he only had two-year survival incidence of 0%. When we made an analysis of 28 studies, we found survival advantage of the total over subtotal resection. (14 vs 11 ).(44)

GBM MRI Recurrence Monitoring sequences.

Glioblastoma Recurrence is not uncommon, so monitoring of recurrence is important, several sequences we have discussed in this article can be used to monitor GBM recurrence, as beside usual MRI sequences that show a well appeared classic lesion, there are sequences can see beyond standard images, here we are to discuss some of these.

MRI Perfusion:  it’s very helpful in detection of GBM recurrence and differentiation between it and effects of radiation.  this is done by monitoring  ADC values differences. by capturing fluid-volume changes in intracellular and extracellular parts of enhanced parts after post-therapy imaging. (45)

Proton MRS: it gives important biochemical details about metabolites of the brain, this help in the diagnosis of the disease and help neurologist to understand the disease. 1.5 T brain MRS currently has a number of clinical applications, one of its most important application is the early diagnosis of GBM recurrence.(46)

DWI: on its images, the necrosis appears heterogeneous spotty and marked hypointense, so that in tumor recurrence, the maximal ADC is lower than in necrosis. (47)

 

 

 

 

 

 

 

 

 

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Here we are finish GBM MRI topic.