Author Archives: Dr Moe.Rad


IMAGING ANATOMY OF PHARYNX & LARYNX is essential to understand subsequent pathology,  The upper aerodigestive tract consists of the pharynx and the larynx. The larynx connects pharynx and trachea.

The pharynx is divided into:

Nasopharynx: extends to inferior portion of  soft palate
Oropharynx: extends from soft palate to hyoid bone
Hypopharynx (laryngeal part of the pharynx): contains pyriform sinuses and posterior pharynx.

The larynx contains:

• The laryngeal surface of epiglottis.                                                                                          • Aryepiglottic folds
• Arytenoid cartilage
• False cords
• True cords (glottis is the space between vocal cords)
• Subglottic larynx

Para-pharyngeal Space    (Fig. 1)

  • it’s Potential space filled with loose connective tissue.
  • A pyramidal Space , with the apex directed toward the lesser cornua of the hyoid bone and the base toward the skull base.
  • It Extends from skull base to mid-oropharynx.
    Lateral: mandible, medial pterygoid muscle
    Medial: superior constrictor muscles of pharynx, tensor and levator veli palatini
    Anterior: buccinator muscle, pterygoid, mandible
    Posterior: carotid sheath.

FIG (1)
  • CONTENTS(Fig. 2)

           • Anterior (prestyloid) compartment : – Internal maxillary artery  – Interior alveolar, lingual, auriculotemporal nerves.

           • Posterior (retrostyloid) compartment:   – ICA, internal jugular vein (IJV) -CNs IX, X, XII -Cervical sympathetic chain lymph nodes.

        • Medial (retropharyngeal) compartment:  Lymph nodes (Rouvière)

FIG (2)
  • Lymphatics (Fig. 3)
    The parapharyngeal space has abundant lymph node groups.
    Lateral pharyngeal node (Rouvière)
    Deep cervical nodes
    Internal jugular chain, including jugulodigastric node
    • Chain of spinal accessory nerve
    • Chain of transverse cervical artery

FIG (3)

Paraganglia (Fig. 4)

Cells of neuroectodermal origin that are sensitive to changes in oxygen and CO2.


• Carotid body (at carotid bifurcation)
• Vagal bodies
Neoplastic transformation of the jugular bulb ganglion produces the glomus jugulare.

FIG (4)

Fluoroscopic Vocal Cord examination (Fig. 5)

Occasionallyperformedtoevaluatethesubglotticregion (Valsalva maneuver), invisible by laryngoscopy.
• Phonation of “E” during expiration: adducts cords.

• Phonation of “reversed E” during inspiration; distends laryngeal ventricles
• Puffed cheeks (modified Valsalva): distends pyriform
• Valsalva: distends subglottic region
• Inspiration: abducts cords.

FIG (5)

Nodal Stations (Fig. 6)

• IA: between anterior margins of the anterior bellies of the digastric muscles, above the
hyoid bone and below the mylohyoid muscle (submental)
• IB: below mylohyoid muscle, above hyoid bone, posterior to anterior belly of digastric muscle,
and anterior to a line drawn tangential to the posterior surface of the submandibular gland
Levels II, III, IV: internal jugular nodes       II: (jugulodigastric) from skull base to lower body of the hyoid bone, through posterior edge of the sternocleidomastoid muscle and posterior edge of the submandibular gland.
Note: A node medial to the carotid artery is classified as a retropharyngeal node.
III: hyoid bone to cricoid cartilage
IV: cricoid to clavicle
Level V: skull base to clavicle, between anterior edge of trapezius muscle and posterior edge of
sternocleidomastoid muscle.

• Level VI: visceral nodes; from hyoid bone, top of manubrium, and between common carotid arteries on each side
• Level VII: caudal to top of the manubrium in superior mediastinum (superior mediastinal

FIG (6)

Pathologic Adenopathy Size Criteria:

Neck lymphadenopathy by size has poor specificity, and no universal standard exists for determination of adenopathy. Nonetheless, two methods are commonly used:
• Long axis: 15mm in levels I and II, 10mm elsewhere
• Short axis: 11mm in level II, 10mm elsewhere Retropharyngeal nodes should not exceed 8mm
(long) or 5mm (short).

Emerging technologies such as MRI lymph node imaging with iron nanoparticles or PET may prove to be more specific and sensitive.


THANKS TO PROF.DR. Ralph Weissleder, MD, PhD



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).


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









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 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 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


  • 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)


(> 6 hours)


(Days to weeks)

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:


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):

(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?


§  Exclude Hge.

§  Early signs of stroke.


§  Intra-cranial circulation.

§  Extra-cranial  circulation


o   PENUMBRA       : Tissue at risk of dying



 Fat suppression is a key consideration in MRI imaging. The following techniques result in fat saturation

  • Short Tau Inversion recovery
  • Spectral pre saturation with inversion recovery
  • Chemical shift selective inversion recovery
  • Dixon method

1) Spectral presaturation with inversion recovery Technique

Spectral pre saturation with inversion recovery technique or SPIR technique is a type of crossbred fat suppression technique(1).

That could acquire an image without fat in it (fat suppression), we can do it by selective protons saturation.

The SPIR technique is useful technique it makes significant attenuation of the fat proton sensitivity while preserving the water proton sensitivity (2).

It uses T1 sequence relaxation and fat frequency excitation then applies of 180-degree radio-frequency inversion pulse to induce a flip angle along the longitudinal axis(3).

This inversion should be followed with a 90-degree excitation pulse which nulls signals of the processing fat molecules as they will not exhibit transverse magnetization hence improving differentiation of pathology.

That could work with RF-pulse fat-selective and also with spoiler gradient, they it ‘s together with residual longitudinal fat magnetization nulling through the mechanism of inversion delay.

the frequency of excitation pulse should be higher than RF pulse (4). This can be helpful only in the fat contenting examed region, as signals coming out of other tissues and water remain unaffected.

2) Chemical shift selective inversion recovery

Chemical shift is the most commonly used technique for fat suppression.

In this technique, we use a selective RF pulse at 90 degrees of narrow bandwidth target processing fat molecules,

so we can process them in the transverse plane (5).

After that immediately gradient spoiler is applied causing them to dephase. Over time imaging sequence begins (d) and no fat signal is seen and the water peak is imaged only (6).

The main disadvantage of this technique is that it should be used at a frequency higher than 1 Tesla and are not working at frequencies less than 0.3 Tesla (7) .

and it should acquire a homogeneous field to work, so we cannot get clear images or findings from an inhomogeneous field like field have a metallic device or any area of abnormal anatomy variants (7).

The main advantage of this technique is that it ‘s very helpful in merging with any pulsed sequences of MRI.

FIGURE (a) to (d) show the different Frequencies of fat suppression selective technique.(8)

Factors that affect chemical shift:

There are two parameters that affect the size of the chemical shift, So in the following sentences, we will discuss the impact of changing these parameters.

Chemical shift artifact is that artifact noticed between fat and water protons due to the difference in the magnetic shields.

it is a powerful artifact which we can use to rule out the existence of lesions consisting of fat  (12).

The artifact of Chemical shift makes dark edge between water and fat interference  (13).

There are several parameters that affect the size of chemical shift artifact including; Magnetic field of the used magnet, gradient strength, and the used bandwidth (14).

the first and most important and crucial parameter is magnetic field strength. In McRobbie et al (2007) textbook, doubling the strength of the magnetic field will increases the chemical shift induced (14).

Moreover, decreasing the gradient strength will increase the chemical shift. Finally, the third parameter that would affect the chemical shift is the bandwidth of the used radio-frequency pulse.

Narrower the bandwidth gives a higher chemical shift while increasing the bandwidth will decrease the chemical shift artifact.



3) Dixon method:


The sequence was named after the man who described it, WT Dixon in 1984(9). It ‘s based on imaging of in and out-of-phase.

we acquire 2 images sets,  the first in-phase TE and the other at out-of-phase TE.

These 2 sets, when added to each other, give ‘water-only’ image while if they subtracted from each other gives ‘fat-only’ image (Fig. below).

So this method is very helpful  in high magnetic susceptibility areas, but it may need magnetic field good homogeneity.(10)

four images of Dixon method, the (A) represent in-phase,(B) represent out-of-phase, (C) represent fat-only, and (D) represent water-only images. (11)

Dixon method has special favors and characters rather than other fat suppression techniques, as its fat signal suppression is less affected by artifacts and more uniform.

also, we can use it with other types of sequences and we can merge ir and use it with different MR sequences, for example, T1 . from a single acquisition, it can give images with or without fat suppression.