Prof.Dr. Fathy Ahmed Tantawy

Zagazig University 

Faculty of Medicine 

Radiology Department 

Imaging of Cerebral Stroke with Different MRI 

Techniques 

By 

Mona Abdel Ghaffar Mohammad Mohammad El-Hariri 

Assistant Lecturer of Radiodiagnosis 



Thesis 

Submitted for Partial Fulfillment of M.D. Degree in Radiodiagnosis 

Supervisors 

Prof.Dr. Fathy Ahmed Tantawy 

Professor of Radiodiagnosis 



Prof.Dr. Dalia Nabil Khalifa 

Professor of Radiodiagnosis 



Prof.Dr. Magdy Abdel Hamead Aidaros 

Assistant Professor of Neurology 





2009

Acknowledgment 

First of all, I would like to thank ALLAH who gives me the 

ability to finish this work. 

I would like to express my profound and greatest gratitude 

and cordial appreciation to Prof. Dr. Fathy Ahmed Tantawy, 

professor of radiodiagnosis, faculty of medicine, Zagazig university 

for his kind encouragement , kind supervision, continuous support 

and beneficial remarks that helped me too much to accomplish this 

work. 

I would like to express my deepest respect to Prof. Dr. Dalia 

Nabil Khalifa, professor of radiodiagnosis, faculty of medicine, 

Zagazig university for her advices and contact observations 

throughout the work. Her encouragement was impetus for 

achievement of the current study. 

I would like to express my sincere thanking and gratitude to 

Prof.Dr. Magdy Abdel Hamead Aidaros, assistant professor of 

Neurology, faculty of medicine, Zagazig university for his help, 

outstanding encouragement that made the accomplishment of this 

work possible. 

I am really grateful to ALL STAFF of Radiodiagnosis 

department , Zagazig university for their continuous encouragement 

and moral support. 

Last, but not least, I would like to record my appreciation and 

gratitude to all my patients, without their kind for their kind help and 

cooperation. 

Mona A. Ghaffar

List of Abbreviations 

2D : two-dimensional. 

3D TOF : three-dimensional time of- flight. 

ACA : Anterior cerebral artery. 

ADC: apparent diffusion coefficient 

AICA : Anterior inferior cerebellar artery. 

AIF : Anterior internal frontal. 

AIS : acute ischemic stroke. 

ASL : arterial spin labelling technique. 

ATP :adenosine triphosphate. 

AVM: Arteriovenous malformation. 

BBB : blood–brain barrier. 

CBF : Cerebral blood flow . 

CBV : cerebral blood volume 

cc: cubic centimeter. 

CE MRA :Contrast-enhanced MRA. 

Ch :choline 

cm: centimeter. 

CNS: central nervous system. 

Cr : creatine. 

CSF: cerebrospinal fluid. 

CSI : Chemical Shift Imaging. 

CT : Computed tomography. 

DWI : Diffusion-Weighted Image. 

EPI : echo planar imaging. 

FLAIR : fluid attenuated inversion recovery. 

FMD : Fibromuscular dysplasia. 

FPol : Frontopolar. 

FSE : fast spin echo. 

g: gram 

GRE : Gradient recalled echo "T2*-weighted images". 

h:hour 

ICA : Internal Carotid Artery. 

ICH : intracranial hemorrhage. 

IIP : Inferior internal parietal . 

IV : Intravenous. 

IVHs : intraventricular hemorrhages. 

Kg: kilogram. 

III 

Abbreviations

III 

Abbreviations 

MCA : middle cerebral artery . 

MI :Myocardial infarction. 

MIF: Middle internal frontal. 

min: minute 

Ml: Mililitre 

mm: millimeter. 

mmol: milimole. 

MRA : magnetic resonance angiography. 

MRI: magnetic resonance Imaging. 

MRS: Magnetic Resonance spectroscopy 

MTT : mean transit time. 

NAA:N-acetylaspartate. 

Na+/ K+ ATPase: Sodium/Potasiam adenosine triphosphatase. 

NCCT: Non Contrast Computed Tomography. 

PC : phase-contrast. 

PCA : Posterior cerebral artery. 

PCT1: post contrast T1. 

PD : proton density . 

PICA : Posterior inferior cerebellar artery. 

PIF : Posterior internal frontal. 

ppm : parts per millions. 

PWI : perfusion weighted images. 

RBCs : Red Blood Cells. 

rCBF : relative Cerebral Blood Flow . 

rCBV : relative Cerebral Blood volume. 

RF pulse: radiofrequency pulse. 

ROI region of interest. 

S: second. 

SAH : Subarachnoid hemorrhage. 

SIP : Superior internal parietal. 

S/N : signal-noise ratio. 

SVS : Single Voxel Spectroscopy. 

T: Tesla. 

TE : echo time 

TGA :Transient global amnesia. 

TIA :transient ischemic attack. 

TR : repetition time. 

TTP : time to peak. 

VOI : volume of interest.

Table of contents 

I 

Table of contents 

Introduction----------------------------------------------------------------------1 

Aim of the work------------------------------------------------------------------3 

Review of literature-------------------------------------------------------------4 

Blood Supply of the Brain----------------------------------------------4 

MRI Anatomy of the brain--------------------------------------------15 

Pathophysiology of stroke---------------------------------------------20 

Conventional MRI in Stroke------------------------------------------26 

Clinical Application of Diffusion Weighted Imaging in Stroke-38 

Clinical Application of Perfusion Weighted Imaging in Stroke-60 

Clinical Application of MRA in Stroke-----------------------------68 

Clinical Application of MRS in Stroke------------------------------75 

Patients and Methods----------------------------------------------------------83 

Results----------------------------------------------------------------------------88 

Illustrative cases---------------------------------------------------------------118 

Discussion-----------------------------------------------------------------------186 

Summary and Conclusion---------------------------------------------------211 

References----------------------------------------------------------------------215 

Arabic summary--------------------------------------------------------------4 -1

Introduction 

- 1 - 

Introduction 

Stroke can be defined as an acute central nervous system injury with 

an abrupt onset (Srinivasan et al.,2006). 

Stroke is a leading cause of mortality and morbidity in the developed 

world. The goals of an imaging evaluation for acute stroke are to establish a 

diagnosis as early as possible and to obtain accurate information about the 

intracranial vasculature and brain perfusion for guidance in selecting the 

appropriate therapy (Srinivasan et al.,2006). 

Acute ischemia constitutes approximately 80% of all strokes and is an 

important cause of morbidity and mortality (Srinivasan et al.,2006). 

Conventional spin-echo MR imaging is more sensitive and more 

specific than CT for the detection of acute cerebral ischemia within the first 

few hours after the onset of stroke (Srinivasan et al.,2006). 

DW imaging is much more sensitive than T2-weighted imaging or 

fluid attenuated inversion recovery (FLAIR) imaging for the detection of 

stroke during the first 6 hours after symptom onset (Kim et al.,2005). 

Diffusion-weighted imaging (DWI) and the apparent diffusion 

coefficient (ADC) are of particular interest, because these parameters show 

changes in ischemic brain tissue within hours after symptom onset, when no 

abnormalities are typically seen on conventional MR images. Acute 

ischemic lesions are characterized by a high signal on DWI and a low ADC. 

The ADC, a measure of the freedom of water diffusion, is believed to be 

low because of a shift of water, within hypoxic brain parenchyma, from the 

extracellular to the intracellular compartment, where water diffusion is 

relatively restricted (Lansberg et al., 2001).

- 2 - 

Introduction 

While diffusion-weighted MR imaging is most useful for detecting 

irreversibly infarcted tissue, perfusion-weighted imaging may be used to 

identify areas of reversible ischemia as well (Srinivasan et al.,2006). 

DW MR imaging depicts infarcted tissue within 5 minutes after the 

occlusion of the feeding vessel. PW imaging is able to depict hypoperfused 

brain tissue around the infarcted core (Karonen et al., 2000). In many 

patients with acute ischemic stroke, the volume of hypoperfused tissue on 

perfusion-weighted maps is larger than the volume of tissue with decreased 

diffusion on diffusion-weighted images. This mismatch between the 

volumes of abnormal tissue on perfusion- and diffusion-weighted images 

(perfusion-diffusion mismatch) in the same imaging session can be 

considered as an estimate of the ischemic penumbra and thus may be a 

predictor of potential infarct growth (Liu et al., 2004). 

The perfusion-diffusion mismatch can be determined by using 

different perfusion parameters, such as relative cerebral blood volume 

(rCBV), relative cerebral blood flow (rCBF), and mean transit time (MTT) 

(Karonen et al., 2000). 

Hydrogen 1 (1H) magnetic resonance (MR) spectroscopy enables 

noninvasive quantification of in vivo metabolite concentrations in the brain 

(Jansen et al, 2006). 

It has become generally accepted that early intracranial hematomas 

typically change over time, mainly, but not exclusively, in two important 

ways that alter MR signal intensity patterns: 1) the oxygenation state of 

hemoglobin changes, and 2) initially intact RBC membranes eventually lyse 

(Ebisu et al., 1997)..

Aim of the work 

-3- 

Aim of the work 

The aim of this work is to assess how we can use different MRI 

techniques in the evaluation of patients having cerebrovascular stroke.

Normal vascular anatomy 

Review of literature 

Fig .18(Weir and Abrahams, 2005) Circle of Willis, arteries of the 

brain with MRA, (a) axial and (b) lateral projection. 

1- anterior cerebral artery. 

2- Anterior communicating artery. 

3- Basilar artery. 

4- Branches( in insula) of the middle cerebral artery. 

5- Cavernous portion of the internal carotid artery. 

6- Cervical portion of the internal carotid artery. 

7- Genu of the middle cerebral artery. 

8- Intracranial (supraclinoid) internal carotid artery. 

9- Middle cerebral artery. 

10- Ophthalmic artery. 

11- Petrous portion of the internal carotid artery. 

12- Posterior cerebral artery. 

13- Posterior cerebral artery in ambient cistern. 

14- Posterior cerebral artery in interpeduncular cistern. 

15- Posterior communicating artery. 

16- Posterior inferior cerebellar artery. 

17- Guadrigeminal portion of posterior cerebral artery. 

18- Superior cerebellar artery.

Fig.1: Arterial supply of the brain-mid sagittal view (Gazzaniga et al., 2002). 

Fig.2: Arterial supply of the brain-lateral view (Gazzaniga et al., 2002). 

Fig.3: Arterial supply of the brain-inferior view (Gazzaniga et al., 2002). 

Review of literature


Fig.4: Blood vessels and cranial nerves at the base of the brain (Tank, 1999). 

Fig.5: Venous drainage of 

the brain (Tank, 1999).

Arterial supply 

- 4 - 


The arterial supply of the CNS is derived from the internal carotid and 

vertebral arteries. All arteries enter the surface of the brain are end arteries, that is, 

they have no precapillary anastmosis with other arteries and obstruction of these 

arteries causes infarct of the supplied territory (Ryan et al, 2004). 

Internal carotid artery 

Once the carotid artery enters the carotid canal it has a very tortuous course- 

six bends in all before its terminal division. 

Branches 

The cervical portion has no branches. Two small branches each arise from 

the petrous and cavernous parts of the internal carotid artery. These are seldom 

visible on angiography. These are: 

The carotictympanic artery to the ear drum. 

The pterygoid artery to the pterygoid canal and plate. 

The cavernous artery to the walls of the cavernous sinus. 

The meningohypophyseal artery, which supplies the dura of the anterior 

cranial fossa and sends branches to the pituitary (Ryan et al, 2004). 

The ophthalmic artery is the first supraclinoid branch of the internal carotid 

artery (Butler et al, 1999). 

The posterior communicating artery runs posteriorly to anastmose with the 

posterior cerebral artery (Ryan et al, 2004). 

The anterior choroidal artery orginates from the posterior aspect of the internal 

carotid artery(Uflacker, 2007). 

Blood Supply of the Brain 

Striate arteries are perforating arteries to the lentiform and the caudate nuclei and 

the internal capsule (Ryan et al, 2004). 

The terminal division of the internal carotid artery is into anterior and 

middle cerebral arteries (Ryan et al, 2004).

The anterior cerebral artery 

- 5 - 


The horizontal portion of the anterior cerebral artery arises anteriorly as the 

smaller of the two terminal branches of the internal carotid artery. It courses 

anteriorly and medially to the interhemispheric fissure. The anterior cerebral artery 

gives origin to two groups of small arteries: an inferior and superior group. The 

small inferior group of branches supplies the superior surface of the optic nerve 

and chiasm and the superior group is formed by the medial striate arteries 

including the artery of Heubner. 

These are 5 to 10 small arteries that supply anterior hypothalamus, the 

septum pellucidum, the medial portion of the anterior commissure, the pillars of 

the fornix and the anterior inferior part of the striatum. (Uflacker, 2007). 

Anterior communicating artery 

The Anterior communicating artery is a very short and communicates both 

anterior cerebral arteries in the interhemispheric fissure. It completes the anterior 

portion of the circle of Willis (Uflacker, 2007). 

Pericallosal artery 

It ascends in front of the lamina terminals, between the two hemispheres 

along the longitudinal fissure, making a curve around the genu of the corpus 

callosum in the pericallosal cistern. 

Segments 

Infracallosal segment. 

Precallosal segment: curved portion of the artery around the genu of the 

corpus callosum. 

Supracallosal segment follows the upper surface of the corpus callosum. 

Branches of the pericallosal artery 

*Orbital artery (Frontobasilar) artery supplies the medial basal region of the 

frontal lobe, including the gyrus rectus, the medial part of the medial gyrus and the 

olfactory bulb and tract. 

*Frontopolar artery arises from the infracallosal segment and supplies anterior 

portion of the medial and lateral surfaces of the superior frontal gyrus. 

*Callosomarginal artery runs over the cingulate gyrus at the cingulated sulcusand

supplys premotor, motor and sensory areas. 

Branches 

Anterior Internal Frontal Artery. 

Middle Internal Frontal Artery. 

Posterior Internal Frontal Artery. 

Paracentral Artery (Uflacker, 2007). 

Cortical Branches of the anterior cerebral artery 

Orbitofrontal (OF). 

Frontopolar (FPol). 

Anterior internal frontal (AIF). 

Middle internal frontal (MIF). 

Posterior internal frontal (PIF). 

Paracentral (PC). 

Superior internal parietal (SIP). 

Inferior internal parietal (IIP) (Uflacker, 2007). 

The middle cerebral artery 

- 6 - 


This is the largest and most direct of the branches of the internal carotid 

artery and is, therefore, the most prone to emblism ((Ryan et al, 2004). 

The middle cerebral artery has been divided into three segments: horizontal, 

sylvian and cortical. The horizontal segment supplies the basal ganglia, the orbital 

surface of the frontal lobe and the temporal lobe. The sylvian segment supplies the 

insula. The cortical branches supply the lateral convexities of the cerebrum 

(Uflacker, 2007). 

Horizontal segment of the middle cerebral artery 

The horizontal segment or M1 of the middle cerebral artery begins at the 

internal carotid bifurcation, runs laterally in the lateral cerebral fissure, and 

terminates entering the sylvian fissure. The junction between the end of the 

horizontal segment and the beginning of the insular segment is known as the 

"knee" of the middle cerebral artery. The horizontal segment of the middle cerebral 

artery bifurcates or trifurcates near the island of Reil in most patients.

The segment M1 presents three main groups of branches: 

Lenticulostriate branches. 

Orbitofrontal branch. 

Anterior temporal arteries. 

Sylvian segment of the middle cerebral artery 

- 7 - 


When passing through the sylvian fissure the several branches of the middle 

cerebral artery feed the insula cortex (Uflacker, 2007). 

Cortical branches of the middle cerebral artery 

The middle cerebral artery supplies the entire superficial lateral surface of 

the cerebral hemisphere in the frontal, temporal, parietal and occipital lobes. 

Branches: 

Orbitofrontal artery. 

Prefrontal artery. 

Precental artery. 

Central arteries. 

Anterior parietal artery. 

Posterior parietal artery. 

Angular artery (terminal artery). 

Tempro-occipital artery. 

Posterior temporal artery. 

Middle temporal artery. 

Anterior temporal artery. 

Temporal polar artery (Uflacker, 2007). 

Vertebrobasilar system 

Vertebral artery 

The vertebral artery arises from the posterosuperior aspect of the first part of 

the subclavian artery.The artery enters the foramen tranversarium of the sixth 

cervical vertebra (occasionally the seventh, fifth or fourth) and ascends through the 

foramina of the upper six (or seven, five or four) cervical vertebrae. It passes 

posterior to the lateral mass of the atlas and enters the skull through the foramen

- 8 - 


magnum. It pierces the dura and arachnoid mater and passes anterior to the 

medulla until it unites with its fellow at the lower border of the pons. 

*In the neck the branches are: 

Spinal branches to the vertebrae and the spinal cord. 

Muscular branches to the deep muscles of the neck. 

*Within the skull the branches are: 

Meningeal branch to the cerebellar fossa and falx. 

Posterior spinal artery descends as two branches anterior and posterior to 

the dorsal roots. 

Anterior spinal artery unites with its fellow anterior to the medulla and 

descends as a single anterior spinal artery. 

Small branches to the medulla oblongata (Ryan et al, 2004). 

Posterior inferior cerebellar artery (PICA): The posterior inferior cerebellar 

artery (PICA) arises from the vertebral artery as its largest and most distal branch. 

The PICA then proceeds to supply the undersurface of the cerebellar hemispheres 

(Butler et al, 1999). 

PICA terminates as: 

The medial branch (inferior vermian artery) to the inferior vermis and 

adjacent inferior surface of the cerebellar hemispheres. 

The lateral branch to the lateral aspect of the inferior surface of the 

cerebellum (Ryan et al, 2004). 

Basilar artery 

Formed by the union of the two vertebral arteries at the lower border of the 

pons, the basilar artery lies close to (but seldom exactly in) the midline, anterior to 

pons in the pontine cistern. 

The branches of the basilar artery are as follow: 

Pontine artery. 

Labyrinthine ( internal auditory artery). 

Anterior inferior cerebellar artery (AICA). It supplies the anterior and 

lateral aspect of the undersurface of the cerebellum. 

Superior cerebellar artery, which arises very close to the terminal division of

- 9 - 


the basilar artery and runs laterally around the cerebellar peduncle of the 

midbrain to the superior surface of the cerebellum which it supplies. This 

artery also sends branches to the pons and the pineal gland. 

Right and left posterior cerebral arteries-the basilar artery teminates by 

dividing into these (Ryan et al, 2004). 

The posterior cerebral arteries 

The posterior cerebral artery receives the posterior communicating artery of 

the internal carotid artery to complete the circle of Willis (Ryan et al, 2004). 

Each posterior cerebral artery can be divided into a number of segments. 

The P1 or the precommunicating segment, extends from the basilar bifurcation to 

the origin of the posterior communicating artery. It lies within the interpeduncular 

fossa and thalamic perforating arteries arise from both this P1 segment and from 

the posterior communicating artery. The P2 or ambient segment, runs around the 

brainstem in the ambient cistern. The P3 segment extends from the quadrigeminal 

plate cistern to the calacrine fissure (Butler et al, 1999). 

The branches of the posterior cerebral artery are as follow: 

Small branches to cerebral peduncle, the posterior thalamus, the medial 

geniculate body and the quadrigeminal plate. 

Thalamostriate arteries: supply the thalamus and the lentiform nucleus. 

Medial and lateral posterior choroidal arteries: supply (with the anterior 

choroidal artery) the choroids plexus of this ventricle. 

Cortical branches are as follow: 

The posterior temporal branch, which supplies the inferior aspect of the 

posterior part of the temporal lobe. 

The internal occipital branch which passes to the medial aspect of the 

occipital lobe and divides terminally into calcarine and parieto-occipital 

arteries (Ryan et al, 2004). 

Circle of Willis (Circulus Arteriosus of Willis) 

Most of the brain is supplied by two internal carotid arteries and the central 

anastomosis between them, called the circle of Willis, which connects the internal

- 10 - 


carotid arteries to the vertebrobasilar system that supplies the remainder brain. The 

circle of Willis is more polygonal than circular. It is located in the cisterna 

interpeduncularis surrounding the optic chiasm, the neural infundibular stem of the 

hypophysis gland, and other neural structures in the interpeduncular fossa. 

Anteriorly the anterior cerebral arteries are joined by the anterior communicating 

artery. Posteriorly the basilar artery divides and orginates the two cerebral arteries, 

and each artery is joined by the ipsilateral internal carotid by a posterior 

communicating artery (Uflacker, 2007). 

Venous Drainage of the brain 

The veins draining the central nervous system do not follow the same 

course as the arteries that supply it. Generally, venous blood drains the nearest 

venous sinus, except in the case of that draining from the deepest structures, which 

drain to deep veins. These drain, in turn, to the venous sinuses (Ryan et al, 2004). 

Venous sinuses 

The venous sinuses of the cranial cavity are blood filled spaces situated 

between the layers of the dura matter, they are lined by endothelium. Their walls 

are thick and composed of fibrous tissue, they have no muscular tissue. The sinuses 

have no valves. They receive tributaries from the brain , the diploe of the skull, the 

orbit and the internal ear (Snell, 2008). 

The superior sagittal sinus starts anteriorly and runs posteriorly in the midline to 

the internal occipital protuberence . Veins enter the sinus obliquely against the 

flow of blood (Ryan et al, 2004) Posteriorly the sinus turns to one side, usually the 

right, to become the transverse sinus (Ryan et al, 2004). 

The inferiorsagittal sinus lies in the free lower margin of the falx cerebri. It joins 

the great cerebral vein to form the straight sinus (Snell, 2008). 

The straight sinus lies at the junction of the falex cerebri with the tentorium 

cerebelli, formed by the union of the inferior sagittal sinus with the great cerebral 

vein. It drains into the transverse sinus (Snell, 2008). 

The transverse and sigmoid sinuses-the transverse sinuses run right and left from 

the confluence of the sinuses to the mastoid bones where they turn inferiorly and

- 11 - 


become the sigmoid sinus, which continues at the jugular foramen as the internal 

jugular vein (Ryan et al, 2004). 

The cavernous sinuses- this sinus is on either side of the pituitary gland connected 

across the midline by the intercavernous sinuses. The cavernous sinus receives the 

ophthalmic vein, the sphenoid sinus and the superficial middle cerebral vein and 

drains via the petrosal sinuses to the sigmoid sinus and the beginning of the 

internal jugular vein (Ryan et al, 2004). 

The superior and inferior petrosal sinuses which run along the upper and lower 

borders of the prtrous part of the temporal bone (Snell, 2008). 

Veins of the brain 

The veins of the brain have no muscular tissue in their thin walls, and they 

possess no valves. They emerge from the brain and drain into the cranial venous 

sinuses (Snell, 2007). 

Superficial cerebral veins: They drain the nearest dural sinus. 

The superior anastomotic vein (of Troland). 

The inferior anastomotic vein (of Labbe). 

The superficial middle cerebral vein (Ryan et al, 2004). 

Deep cerebral veins 

Three veins unit just behind the interventricular foramen (of Monoro) to 

form the internal cerebral vein. These are: 

The choroids vein. 

The septal vein. 

The thalamostriate vein. 

The point of union of these veins is called the venous angle. 

The internal cerebral veins of each side unit to from the great cerebral vein. 

The great cerebral vein (of Galen) receives the basal veins and posterior fossa 

veins and drains to the anterior end of the straight sinus. 

The basal vein (of Rosenthal) begins to the anterior perforated substance by the 

union of three veins: 

The anterior cerebral vein. 

The deep middle cerebral vein.

The striate veins from the basal ganglia. 

- 12 - 


The basal vein of each side passes around the midbrain to join the great cerebral 

vein (Ryan et al, 2004). 

Veins of the posterior fossa 

The anterior pontomesencephalic vein. 

The posterior mesencephalic vein. 

The precentral cerebellar vein. 

The superior vermian vein drains also to the great vein while the inferior vermian 

veins (paired) drain to the sagittal sinus (Ryan et al, 2004).

- 13 - 


- 14 - 


- 15 - 


MR sectional anatomy of the brain (Brant and Helms, 

2007) 

MRI ANATOMY OF THE BRAIN 

Normal axial MRI anatomy [figure 6 to 17].

- 16 - 


- 17 - 


- 18 - 


- 19 - 


- 20 - 


Stroke is and has been the third leading cause of death in most countries 

around the world for a very long time (Caplan, 2006). 

Although strokes are much more common in people over 65, and many 

people believe that strokes only happen to old folks, strokes can occur at any age, 

including infancy, childhood, adolescence and early adulthood (Caplan, 2006). 

The brain, and every other organ in the body depends on a constant supply 

of energy to function normally. Fuel for the brain is carried in the blood. The brain 

requires more fuel than any other organ in the body. The two main energy sources 

that the brain uses are sugar and oxygen. Oxygen is carried mainly in the 

hemoglobin of red blood cells; sugar is carried in the serum of the blood. When a 

part of the brain does not receive an adequate supply of the blood, or when the 

blood does not carry enough oxygen or sugar, that portion of the brain becomes 

unable to perform its normal functions. Stroke is a term that is used to describe 

brain injury caused by abnormality of the blood supply to apart of the brain 

(Caplan, 2006). 

Strokes can be divided into two very broad groups: hemorrhage and 

ischemia. Hemorrhage refers to bleeding inside the skull, either into the brain or 

into the fluid surrounding the brain. The second major types of strokes are called 

ischemia, a term that refers to lack of blood. (Caplan, 2006).Cerebral infarction 

accounts for approximately 85% of all strokes (Haaga et al, 2003). 

Causes of Stroke: 

a) Ischemic Stroke according to (Torbey and selim, 2007) 

1)Cardiac embolism 

Conditions have been associated with an increased risk of ischemic stroke from 

cardioembolism. 

Acute myocardial infarction (AMI). 

CHF. 

PATHOPHYSIOLOGY OF STROKE 

Atrial Fibrillation.

Patent foramen ovale and paradoxical emboli. 

Valvular disease. 

2) Artery to artery embolism 

- 21 - 


Embolic material is derived from sources distal to the aortic valve in artery 

to artery embolism. This material subsequently mobilizes distal to its site of origin. 

1) Atheroemboli in large and medium artery atherosclerotic disease. 

2) Aortic arch atheromatous disease. 

3) Arterial dissection. 

4) Arterial thrombus formation in hypercoagulable states. 

5) Large vessel arteriopathy associated with sickle cell disease. 

6) Cardiothoracic surgery 

3) Small artery occlusive disease, lacunar infarction 

Lacunar infarcts are small, deep cerebral infarcts, most often encountered 

in the setting of hypertension. These infarcts result from occlusion of very small 

penetrating branches (Brown et al., 1988). 

4) Hypoperfusion and hypoxemia 

Some causes of decreased systemic perfusion and hypoxic states include 

sepsis, intraoperative hypotension,cardiopulmonary arrest,cardiac arrhythmia, 

volume depletion and antihypertensive medication. 

5) Thrombotic stroke and hypercoagulable states. 

Other Causes 

1- Vasospasm as subarchnoid hemorrhage related contribute to ischemic event, 

especially with the presence of a distal arterial stenosis (Torbey and selim, 2007). 

2- Venous sinus thrombosis (Gonzalez et al., 2006). 

3- Migraine (Gonzalez et al., 2006). 

b) Hemorrhagic Stroke 

1) Intracerebral hemorrhage (Torbey and selim, 2007). 

a) Traumatic ( cerebral contusion). 

b) Spontaneous (non traumatic). 

1- Hypertension.

2- Amyloid angiopathy. 

3- Vascular malformations . 

4- Intracranial aneurysms. 

5- Arterial thrombosis( hemorrhagic transformation). 

6- Venous thrombosis (dural sinuses or deep venous system). 

7- Coagulopathy 

8- Neoplastic as leukemia. 

9- Vasculitis (Torbey and selim, 2007). 

2) Subarachnoid hemorrhages 

a) Arterial aneurysm. 

b) Vascular malformations near the brain surface. 

c) Bleeding tendancies. 

d) Head injury. 

3) Subdural hemorrhages 

4) Epidural hemorrhages (Caplan, 2006). 

Mechanism of ischemia 

- 22 - 


Focal cerebral ischemia differs from global ischemia. In global ischemia 

irreversible neuronal damage occurs after 4–8 min at normal body temperature. In 

focal cerebral ischemia collateral vessels almost always provide some degree of 

residual blood flow, which may be insufficient to preserve neuronal survival. 

Location of arterial occlusion affects the impairment of cerebral function: 

Obstruction below the circle of Willis often permits collateral flow through the 

anterior or the posterior communicating arteries. Vertebral artery obstruction can 

be bypassed through small deep cervical arteries. In obstructions of the cervical 

internal carotid artery, limited collateral flow can be provided through external 

carotid artery branches such as the periorbital or the ethmoidal arteries. Collateral 

flow mainly derives from the arteries of the circle of Willis. 

Basically, the loss of oxygen and glucose supply results in the collapse of 

cellular energy production with subsequent changes in cellular metabolism, 

degradation of cell membranes, and finally necrosis. 

The margins of the infarction are usually hyperemic due to activated

- 23 - 


meningeal collaterals. The ischemic tissue swells rapidly because of increased 

intracellular water content. During ischemia, the arteries first dilate to increase 

blood supply to the oligemic tissue, but will subsequently constrict due to ischemic 

damage. Reperfusion may then lead to hyperemia due to impaired autoregulative 

capacity of the damaged arteries. In prolonged ischemia sludging and endothelial 

damage will prevent reperfusion (Kummer and Back, 2006). 

Unlike muscle, brain tissue is exquisitely sensitive to ischemia, because of 

the absence of neuronal energy stores. In the complete absence of blood flow, the 

available energy can maintain neuronal viability for approximately 2–3 minutes 

(Srinivasan et al, 2006). 

Two main factors dictate whether brain tissue subjected to hypoperfusion 

becomes necrotic: the magnitude and the duration of cerebral hypoperfusion. The 

former is the most important. Normal cerebral blood flow is 55ml/100g per minute 

(Wityk and Llinas, 2006). 

It appears that the first result of ischemia is an alteration of the cellular 

metabolism from an aerobic to an anaerobic state. This produces increased 

intracellular lactate with a concomitant decrease in intracellular ATP. This 

decrease in the energy stores of the cell leads to a number of physiological 

changes, including decreased pH, increased extracellular potassium, and/ or 

increased extracellular neurotransmitters (glutamate) (Sorensen and Reimer, 

2000). 

With the loss of ATP production, Na + / K + ATPase, an enzyme that is 

important to cell homeostasis, fails. This events permits the unbalanced influx of 

extracellular calcium and sodium and secondarily, the influx of extracellular water 

into cells. This increased intracellular water is termed cytotoxic oedema (Haaga et 

al, 2003). 

Ischemic penumbra 

Brain tissue is exquisitely vulnerable to ischemia. In the complete absence 

of blood flow, available energy stores can maintain neuronal activity for only a 

couple of minutes. However, in the event of an acute ischemic stroke, the ischemia 

is often incomplete, with the injured areas of the brain continuing to receive blood

- 24 - 


from uninjured arterial and leptomeningeal collaterals. The result is a central zone 

of completely infracted tissue referred to as the "core" surrounded by a peripheral 

zone of ischemic but salvageable tissue referred to as the "penumbra' (Sanghvi et 

al., 2007). 

The ischemic penumbra is defined as functionally impaired but salvageable 

ischemic brain tissue surrounding an irreversibly damaged core1 and is the target 

of most recen ttreatments for acute stroke (Oppenheim et al, 2001). 

Evoked potentials in the peripheral region are abnormal, and the cells have 

ceased to function, but this region is potentially salvageable with early 

recanalization. The transition from ischemia to irreversible infarction depends on 

both the severity and the duration of the diminution of blood flow. (Srinivasan et 

al, 2006). 

b) Hemorrhagic Stroke 

Intracerebral hemorrhage 

Bleeding into the brain results from rupture of small blood vessels- the 

arterioles and capillaries within the brain substance. Intracerebral hemorrhage is 

most often caused by uncontrolled hypertension. The blood usually oozes into the 

brain under pressure and forms a localized, blood collection called a hematoma. 

Hematoma exert pressure on brain regions adjacent to the collection of blood and 

can injure these tissues. Large hemorrhages are often fatal because they increase 

pressure within the skull squeezing vital regions within the brain stem (Caplan, 

2006). 

Subarachnoid hemorrhage 

Bleeding into the fluid around the brain is called subarachnoid hemorrhage, 

because blood collects and stays under the arachnoid membrane that lies over the 

pia mater. Subarachnoid hemorrhages are usually caused by rupture of of an 

aneurysm. The artery breaks, spilling blood instantly into the spinal fluid that 

circulates around the brain and spinal cord. The sudden release of blood under high 

pressure increases the pressure inside the skull and causes sever, sudden onset 

headache, often with vomiting. The sudden increase in pressure causes a lapse in 

brain function (Caplan, 2006).

- 25 - 


1) Ischemic Stroke 

- 26 - 


Conventional spin-echo MR imaging is more sensitive and more specific 

than CT for the detection of acute cerebral ischemia within the first few hours after 

the onset of stroke (Srinivasan et al, 2006). 

Conventional spin-echo MRI is more sensitive to the accumulation of tissue 

water than CT and this increased tissue water content due to edema provides the 

signal contrast in ischemic parenchyma on MR imaging. However, the MR image 

is often normal in the first 8 hours and gradually becomes more hyperintense 

during the first 24 hours (Rima et al., 2003). 

Strokes have a characteristic appearance on conventional MRI that varies 

with infarct age. Temporal evolution of strokes is typically categorized into 

hyperacute (0–6 h), acute (6–24 h), subacute (24 h to approximately 2 weeks), and 

chronic stroke (>2 weeks old) (Gonzalez et al., 2006). 

Hyperacute Infarction 

In the hyperacute period (first 6 h), there is shift of water from the 

extracellular to the intracellular space but there may be little increase in overall 

tissue water (Gonzalez et al., 2006). 

Conventional MRI in Stroke 

If imaging is initiated within the first 6 hours, during which time cytotoxic 

edema predominates, standard T2- and T1-weighted images are completely normal 

in the majority of cases. In a minority of cases careful scrutiny of the T1-weighted 

images may show subtle evidence of mass effect (Davis et al, 2003). 

In the hyperacute stage of infarct, there is occlusion or slow flow in the 

vessels supplying the area of infracted tissue. Within minutes of the infarct, the 

signal flow void on T2-weighted images is lost. Increased signal intensity in the 

lumen of large and small vessels may be observed on FLAIR images as the only 

indication of infarction, a finding that has been called the “hyperintense vessel 

sign” or arterial hyperintensity. The physiopathologic basis of this phenomenon

- 27 - 


remains unclear. Several hypotheses have been proposed, such as slowly moving 

or stationary blood, intraluminal thrombus or embolus, or even retrograde 

collateral circulation (Makkat et al., 2002). 

Absence of the normal flow void signal is seen in either or both T1- and T2- 

weighted scans. This sign is more easily identified in the larger vessels of the 

Circle of Willis and the M1 and M2 segments of the middle cerebral artery. When 

present in the middle cerebral artery, this sign can be regarded as the MRI 

equivalent of the dense middle cerebral artery sign, as seen with CT (Davis et al, 

2003). 

Gradient recalled echo (GRE) T2*-weighted images can detect an 

intraluminal thrombus (deoxyhemoglobin) in hyperacute infarcts as a linear low 

signal region of magnetic susceptibility (Gonzalez et al., 2006). 

Contrast-enhanced T1-weighted images show arterial enhancement in 50% 

of hyperacute strokes. This arterial enhancement is thought to be secondary to slow 

flow, collateral flow or hyperperfusion following early recanalization. It may be 

detected as early as 2 h after stroke onset and can persist for up to 7 days. During 

this period, there is usually no parenchymal enhancement because inadequate 

collateral circulation prevents contrast from reaching the infarcted tissue. Rarely, 

early parenchymal enhancement may occur when there is early reperfusion or good 

collateralization (Gonzalez et al., 2006). 

Acute infarction: 

By 24 h, as the overall tissue water content increases due to vasogenic 

edema following blood–brain barrier disruption, conventional MRI becomes more 

sensitive for the detection of parenchymal infarcts (Gonzalez et al., 2006). 

Water is also associated with longer T1 and T2 relaxation times than those 

for normal brain tissue. Therefore, one effect of cytotoxic oedema on MRI scans is 

to increase the T1 and T2 relaxation times of the involved tissues. Although 

regions of the brain that are involved with ischemic stroke may be depicted as 

areas of relative T1 and T2 prolongation, the changes on a T1-weighted image are 

not usually seen as early as the changes on T2-weighted images. In the acute stroke 

patient, the earliest findings on conventional MRI scans are regions of increased

signal intensity on long repetition time (TR) images (Haaga et al, 2003). 

- 28 - 


Signal changes during the first 24 h are best appreciated in the cortical and 

deep gray matter. Infarcts in the acute stage usually demonstrate focal or confluent 

areas of T2 and FLAIR hyperintensity with sulcal effacement. During this time, the 

white matter may be hyperintense, but also may show no abnormality or 

demonstrate hypointensity. Proposed etiologies for the subcortical white matter 

hypointensity are free radicals, sludging of deoxygenated red blood cells, and iron 

deposition. Because cerebrospinal fluid (CSF) is hypointense, FLAIR has 

improved detection of small infarctions in brain parenchyma, such as cortex and 

periventricular white matter, adjacent to CSF. By 24 h, T2-weighted and FLAIR 

weighted images detect 90% of infarcts. An increase in tissue water also leads to 

hypointensity on T1-weighted images. However, in the acute period, T1-weighted 

images are relatively insensitive at detecting parenchymal changes compared with 

T2- weighted images. At 24 h, sensitivity is still only approximately 50% 

(Gonzalez et al., 2006). 

Cytotoxic oedema can also influence the appearance of brain tissues on 

imaging studies by creating regional mass effect. In acute stroke cases involving 

the cortex of the brain, stroke-related edema is commonly associated with swelling 

of the cortical gyri. Gyral swelling is typically identified on imaging studies by the 

observation that the sulci between the gyri are effaced (i.e., narrowed). Regional 

sulcal effacement is, therefore, a sign that can be used to detect the changes of 

acute stroke (Haaga et al, 2003). 

Subacute infarction: 

In the subacute phase of infarct (1 day to 2 weeks), the increase in 

vasogenic edema results in increased T2 and FLAIR hyperintensity, increased T1 

hypointensity, and better definition of the infarction and swelling. The brain 

swelling is manifest as gyral thickening, effacement of sulci and cisterns, 

effacement of adjacent ventricles, midline shift, and brain herniation. The swelling 

reaches a maximum at about 3 days and resolves by 7–10 days. There is increased 

T2 and FLAIR signal within the first week that usually persists but there may be 

“MR fogging”. MR fogging occurs when the infarcted tissue becomes difficult to

- 29 - 


see because it has developed a signal intensity similar to that of normal tissue 


The causes of fogging are not clear, but it has been proposed that a decrease 

in oedema, accompanied by increase macrophage activity, may be responsible. In 

such cases, parenchymal enhancement on T1-weighted images is typically seen 

after injection of gadolinium contrast material (Haaga et al, 2003). 

In the subacute phase, arterial enhancement peaks at 1–3 days. Large 

infarcts will also demonstrate meningeal enhancement that may represent reactive 

hyperemia, which peaks at 2–6 days. Arterial and meningeal enhancement both 

typically resolve by 1 week. In addition, parenchymal enhancement occurs during 

this phase. Gray matter enhancement can appear band-like or gyriform. This is 

secondary to disruption of the blood–brain barrier and restored tissue perfusion 

from a recanalized occlusion or collateral flow. This parenchymal enhancement 

may be visible at 2–3 days but is consistently present at 6 days and persists for 6–8 

weeks. Some infarcts, such as watershed and non cortical infarcts may enhance 

earlier(Gonzalez et al., 2006). 

Chronic Infarcts 

After 2 weeks, the mass effect and edema within infarcts decrease and the 

parenchyma develops tissue loss and gliosis. During this time, parenchymal 

enhancement peaks at 1–4 weeks and then gradually fades. The chronic stage of 

infarction is well established by 6 weeks. At this point, necrotic tissue and edema 

are resorbed, the gliotic reaction is complete, the blood–brain barrier is intact, and 

reperfusion is established . There is no longer parenchymal, meningeal or vascular 

enhancement, and the vessels are no longer hyperintense on FLAIR images. There 

is tissue loss with ventricular, sulcal, and cisternal enlargement. There is increased 

T2 hyperintensity and T1 hypointensity due to increased water content associated 

with cystic cavitation .With large middle cerebral artery (MCA) territory 

infarctions, there is Wallerian degeneration, characterized by T2 hyperintensity and 

tissue loss, of the ipsilateral cortical spinal tract (Gonzalez et al., 2006). 

In some cases, areas of gyral increased density and increased signal on T1- 

weighted images may appear to reflect mineralization (i.e. calcification) within

areas of cortical necrosis (Haaga et al, 2003). 

Finally: 

- 30 - 


Standard MRI sequences are extremely sensitive to the detection of acute, 

subacute and chronic infarcts. However, standard sequences are negative in the 

majority of infarcts (within the first 6–8 hours). Sensitivity is increased by the use 

of contrast enhancement and FLAIR, but accurate diagnosis of hyperacute 

infarction depends on the use of diffusion-weighted imaging (Davis et al, 2003). 

2) Hemorrhagic Stroke 

Non-traumatic intracranial hemorrhage (ICH) accounts for 10–15% of all 

strokes, but up to 25% of more severe strokes. In the hyperacute emergency 

assessment (< 6–12 h) computed tomography (CT) is the diagnostic standard and 

modality of choice to differentiate between hyperacute ICH and ischemic stroke. 

In general, MRI at this stage is considered to be of little value for the diagnosis of 

intracerebral or subarachnoidal hemorrhage and many authors claim that the 

sensitivity of MRI for detecting hyperacute ICH is poor. While hyperacute ICH is 

hyperdense on acute CT scans with progressing time and hematoma degradation, 

there is a loss of density and the ICH may appear isodense or hypodense. MRI is 

far superior to CT in the subacute and chronic stages especially with regard to 

concomitant or underlying pathology. 

The ability to detect acute hemorrhage by MRI is related to the oxygen 

saturation of hemoglobin and its degradation. As a hematoma ages, the hemoglobin 

passes through several forms (oxyhemoglobin, deoxyhemoglobin, and 

methemoglobin) prior to red cell lysis and breakdown into ferritin and hemosiderin 

(Davis et al, 2003). 

The Evolution of MR Signals in ICH 

Based on the most mature form of the hemoglobin present in the clot, five 

stages of evolving ICH have been described. The hyperacute stage lasts for 24 h, 

acute stage for 2–3 days, early subacute stage for 3–7 days, late subacute stage up 

to 2 weeks and chronic stage more than 2 weeks. The evolution of an ICH is a 

complex and dynamic process and the estimation of the time of onset based on 

MRI findings may be inaccurate (Kummer and Back, 2006).

Hyperacute ICH 

- 31 - 


Hyperacute stroke does not demand a complete diagnostic workup, with 

which all the important pathophysiologic aspects of hyperacute ischemic stroke 

can be investigated but also differentiation between ischemic stroke and intra- 

cranial hemorrhage by the radiologist, which is impossible by clinical means only 

(Fiebach and Schellinger, 2003). 

It was initially believed that on MRI an ICH of less than 24 h duration could 

not be distinguished reliably either from a mass lesion or from an acute infarct, 

because of an unspecific pattern of isointensity in T1 and slight hyperintensity on 

T2 imparted by the predominance of oxyhemoglobin. However, due to a reduced 

oxygen tension at the periphery of the clot, some deoxygenation of hemoglobin 

occurs immediately after the bleeding, and several studies have demonstrated that 

the resulting susceptibility effects can be visualized very early on T2- and 

particularly on T2*-weighted images as a hypointense rim . This finding may be 

less apparent or even not apparent at all with low-field systems, or if FSE T2 

sequences are used. It was reported that the ability of high field MRI to reliably 

detect a spontaneous ICH as early as 20 min after onset and schematized the 

appearance of the hyperacute hemorrhage as consisting of three distinct concentric 

regions. The center of the hemorrhage appears isointense or heterogeneously 

hyperintense on T2- and T2*-weighted images, probably reflecting the presence of 

intact oxyhemoglobin. The periphery is hypointense on T2- and T2*-weighted images 

reflecting the susceptibility effects due to deoxyhemoglobin, and finally there is an outer 

rim that appears hypointense on T1-weighted images and hyperintense on T2- and T2*weighted 

images, suggestive of edema (Kummer and Back, 2006). 

Acute ICH 

In the absence of rebleeding, deoxygenation of the clot is completed in most 

cases by 24 h. At that time deoxyhemoglobin becomes the predominant blood 

breakdown product in the lesion. Due to its paramagnetic properties and its 

compartmentalization within still intact RBCs, deoxyhemoglobin exerts a strong 

susceptibility effect, which makes acute hematomas appear distinctly and 

characteristically dark on T2 weighted SE images, and more so on T2* weighted

- 32 - 


GRE images . On T1-weighted images, acute ICHs still appear isointense or mildly 

hypointense, as in the hyperacute stage. The parenchyma surrounding the clot 

exhibits a halo due to vasogenic edema and initial inflammatory reaction. The 

region of edema has long T1 and T2 relaxation times and appears hypointense on 

T1-weighted images and hyperintense on T2-weighted images. Edema is better 

shown by T2-weighted SE sequences than by T2* sequences. By the 5th to 12th 

day the hyperintense halo from edema begins to regress. These features of acute 

ICH last for about 3 days, after which formation of methemoglobin from 

deoxyhemoglobin begins and the clot evolves into the subacute stage(Kummer and 

Back, 2006). 

Early and Late Subacute ICH 

The appearance of methemoglobin in the clot marks the transition from the 

acute to the subacute phase. Too high or too low oxygen tension is likely to delay 

methemoglobin formation and the expected evolutionary changes of ICH. Unlike 

deoxyhemoglobin, methemoglobin allows water protons to approach the 

paramagnetic ion. This is possible due to a conformational change occurring in the 

structure of methemoglobin, which brings the ferric ion to the surface of the 

molecule. With this change PEDD interaction becomes possible and leads to the 

shortening of T1 that is characteristic of subacute hematomas. Since 

methemoglobin is formed initially at the interface of the hematoma with the 

parenchyma of the brain, the bright signals on T1-weighted images are observed 

initially at the periphery of the clot. Later, the bright signal extends centripetally 

until the whole clot becomes hyperintense in T1. This paramagnetic T1 shortening 

effect is observed at all field strengths. In the early subacute phase, methemoglobin 

is still compartmentalized within red blood cells and hence generates local field 

gradients that maintain a T2 shortening effect similar to that induced by 

deoxyhemoglobin. Therefore, in the early subacute phase relaxivity effects and 

susceptibility effects coexist, i.e. the clot appears bright in T1, and dark in T2 and 

especially in T2*. This stage is expected to last for approximately 1 week. As the 

clot ages, progressive fragmentation and osmotic phenomena damage RBC 

membranes until they eventually lyse. Hemolysis releases methemoglobin into the

- 33 - 


extracellular fluid compartment of the hematoma. The resulting dilution of 

methemoglobin in the extracellular fluids eliminates the biological field gradients, 

and with them the susceptibility phenomena, an effect that is observed initially at 

the periphery of the clot. When all methemoglobin is extracellular, the T2- 

shortening induced signal loss is no longer observed, so that the late subacute ICH 

is predominantly hyperintense in both T1- and T2-weighted images. Focal brain 

lesions containing fat, calcium, or high concentrations of proteins can also appear 

hyperintense in T1 and T2 and therefore enter in the differential diagnosis of ICH 

at this stage (Kummer and Back, 2006). 

Chronic ICH 

The beginning of the chronic phase is characterized by the appearance of 

modified macrophages (microglia), which phagocytose the ferritin and the 

hemosiderin formed from the breakdown of extracellular methemoglobin. These 

macrophages accumulate at the periphery of the hematoma and form a ring around 

the remnants of the clot. Hemosiderin is highly paramagnetic as it has five 

unpaired electrons. Its location inside the lysosomes of macrophages is responsible 

for the creation of field gradients and of marked T2 shortening. Hemosiderin is 

also insoluble in water, which prevents PEDD interaction. In the absence of T1 

shortening no bright signals are observed from hemosiderin on T1-weighted 

images. However, at the beginning of the chronic stage there may still be free 

methemoglobin in the center of the clot giving bright signals on T1-weighted 

images. As a result, a chronic ICH initially shows a hypointense peripheral 

hemosiderin rim completely surrounding a central area hyperintense in all 

sequences due to the persistence of extracellular methemoglobin. The hemosiderin 

rim is less conspicuous on T1-weighted sequences and more conspicuous on T2- 

and T2*-weighted sequences. With time, the macromolecules in the hematoma 

cavity are slowly reabsorbed. This results in a gradual disappearance of 

paramagnetic T1 shortening effects. With the elimination of all macromolecular 

components, the lesion becomes more fluid and the signal intensity of the inner 

part of the clot becomes isointense to CSF in all sequences. Finally, the cyst-like 

cavity collapses leaving a residual hemosiderin-containing scar (Kummer and

What 

happens 

Back, 2006). 

- 34 - 


Table 1: (Reimer et al., 2006:) Sequential signal intensity (SI) changes of intracranial 

haemorrhage on MR imaging (1.5 T). 

Hyperacute Acute haemorrhage Early subacute Late subacute Chronic haemorrhage 

haemorrhage 

haemorrhage haemorrhage 

Blood leaves the 

vascular system 

(extravasation) 

Deoxygenation with 

formation of deoxy- 

Hb 

Time frame

- 35 - 


CT is also the (imaging) standard of care for the diagnosis of acute 

subarachnoid hemorrhage with a sensitivity of 85–100%. The CT-based diagnosis 

of SAH may be difficult in the posterior fossa due to bone artefacts as well as with 

small amounts of blood. In the subacute stage the sensitivity of CT for SAH 

diminishes substantially with sensitivities of 50% after 1 week, 30% after 2 weeks 

and ≈0% at 3 weeks necessitating the diagnostic gold standard in SAH, i.e. lumbar 

puncture. There currently is only scarce information about the sensitivity of stroke 

MRI for SAH. Initial assumptions that MRI may also be suitable in the diagnosis 

of acute SAH were derived from in vitro studies (Fiebach and Schellinger, 2003). 

CT shows the acute SAH as high attenuation areas filling the cisterns and 

sulci (Kummer and Back, 2006). 

Conventional T1–WI and T2–WI were shown to be ineffective in the 

diagnosis of acute SAH with sensitivities of 35–50%. This may, in part, be due to 

the fact that the rules, which apply for intracerebral degradation of ICH, may not 

be valid for SAH due to a higher oxygen partial pressure in cerebrospinal fluid 

(CSF) and that the formation of blood clots which also causes T2-shortening is 

impaired. The paramagnetic susceptibility effect, which may be utilized to detect 

intracerebral hemorrhage, is not suitable for the detection of SAH as the latter 

frequently is localized in the vicinity of the cranial vault or skull base, thus areas 

which are prone to artifacts. The detection of SAH may be improved by using PD– 

WI with shorter repetition times (TR) to visualize the T1-effect. FLAIR sequences 

have been reported to be suitable for the diagnosis of not only subacute but also 

acute SAH (Davis et al, 2003) 

In subacute SAH (5days to 2 weeks) MRI with fluid attenuated inversion 

recovery (FLAIR) sequences and proton density (PD) weighted images is clearly 

superior to CT (sensitivity 100% vs. 45%) (Davis et al, 2003). 

In FLAIR an inversion pulse is utilized to null the bright CSF signals in T2- 

weighted images with long TE. Due to its high protein concentration and T1 

shortening effect, the acute subarachnoid bleeding will appear bright on FLAIR. 

While FLAIR may be very sensitive in the detection of acute SAH, its specificity 

for this disease is suboptimal. All conditions causing an elevation of CSF proteins,

- 36 - 


such as pyogenic meningitis, granulomatous meningitis, meningeal carcinomatosis 

etc., characteristically elevate the CSF protein levels and give rise to bright signals 

on FLAIR. Fat from ruptured dermoid or previous introduction of oily contrast 

media may also mimic SAH on FLAIR due to T1 shortening effects. Therefore, in 

order to confidently make a diagnosis of SAH on FLAIR, a careful appraisal of the 

clinical history is mandatory. Contrast may be helpful to exclude meningitis, while 

fat may be identified using chemical shift artifacts or fat saturation sequences. 

Another pitfall with FLAIR sequences may be represented by the CSF pulsation 

artifacts from inflow and misregistration effects. These artifacts create bright 

signals in the cisterns especially with fast FLAIR sequences. Hence, FLAIR may 

not be suitable to assess the posterior fossa SAH. Proton density-weighted images 

seem to be as sensitive as FLAIR in detecting SAHs of less than 24 h. CSF flow 

artifacts in cisterns and ventricles are less likely to be observed with proton density 

than with FLAIR (Kummer and Back, 2006). 

Intraventricular Hemorrhage 

Most intraventricular hemorrhages (IVHs) are secondary to ICH or SAH. 

Isolated IVH is rare and usually due to the rupture of underlying vascular 

malformations. Based on MR imaging, intraventricular bleedings have been 

classified into clotted IVH, usually unilateral, and layered IVH, usually bilateral. 

Since the CSF in ventricles has a higher content in oxygen and glucose, the layered 

form evolves more slowly compared to the clotted form. The latter evolves at a rate 

similar to ICH. However, in the chronic stage, unlike ICH, IVHs do not show 

hemosiderin formation. Among the conventional sequences, proton density depicts 

IVH better than T1- and T2-weighted images. In the acute stage FLAIR may have 

better sensitivity than CT scan to demonstrate IVH. On FLAIR, in the initial 48 h 

IVH appears hyperintense, but one should be aware of the CSF flow artifacts, 

which can mimic the presence of blood. Also, conditions like pyocephalus or 

intraventricular tumors may exhibit signals similar to IVH. After the acute phase, 

IVHs may appear iso- or hypointense on FLAIR. At this stage, a bright signal on 

T1-weighted images and a hypointense signal on T2*-weighted image will mark 

the presence of an IVH (Kummer and Back, 2006).

- 37 - 


Clinical Application of Diffusion Weighted 

Imaging in Stroke 

- 38 - 


Diffusion weighted imaging is an MR imaging technique in which contrast 

within the image is based on microscopic motion of water (Rajeshkannan et 

al.,2006). 

Diffusion-weighted (DW) magnetic resonance (MR) imaging provides 

potentially unique information on the viability of brain tissue. It provides image 

contrast that is dependent on the molecular motion of water, which may be 

substantially altered by disease. Stejskal and Tanner provided an early description 

of a DW sequence in 1965. They used a spin-echo T2-weighted pulse sequence 

with two extra gradient pulses that were equal in magnitude and opposite in 

direction. This sequence enabled the measurement of net water movement in one 

direction at a time. To measure the rate of movement along one direction, for 

example the x direction, these two extra gradients are equal in magnitude but 

opposite in direction for all points at the same x location. However, the strength of 

these two balanced gradients increases along the x direction. Therefore, if a voxel 

of tissue contains water that has no net movement in the x direction, the two 

balanced gradients cancel each other out. The resultant signal intensity of that 

voxel is equal to its signal intensity on an image obtained with the same sequence 

without the DW gradients. However, if water molecules have a net movement in 

the x direction (eg, due to diffusion), they are subjected to the first gradient pulse at 

one x location and the second pulse at a different x location. The two gradients are 

no longer equal in magnitude and no longer cancel. The difference in gradient 

pulse magnitude is proportional to the net displacement in the x direction that 

occurs between the two gradient pulses, and faster-moving water protons undergo 

a larger net dephasing. The resultant signal intensity of a voxel of tissue containing 

moving protons is equal to its signal intensity on a T2-weighted image decreased

- 39 - 


by an amount related to the rate of diffusion. The signal intensity (SI) of a voxel 

oftissue is calculated as follows: 

SI= SI0 x exp (-bx D). 

where SI0 is the signal intensity on theT2-weighted (or b = 0 sec/mm2) image,the 

diffusion sensitivity factor b is equal 

toγ 2 G 2 δ 2 (∆-δ /3), and D is the diffusion coefficient. γ is the gyromagnetic ratio; G 

is the magnitude of δ, the width of, and ∆ is the time between the two balanced 

DW gradient pulses. When measuring molecular motion with DW imaging, only 

the apparent diffusion coefficient (ADC) can be calculated. The signal intensity of 

a DW image is best expressed as: 

SI = SI0 x exp (-bx3 ADC). 

In the brain, apparent diffusion is not isotropic (the same in all directions); it is 

anisotropic (varies in different directions),particularly in white matter. The cause 

of the anisotropic nature of white matter is not completely understood, but 

increasing anisotropy has also been noted in the developing brain before T1-and 

T2-weighted imaging or histologic evidence of myelination becomes evident. It is 

likely that in addition to axonal direction and myelination, other physiologic 

processes, such as axolemmelic flow, extracellular bulk flow, capillary blood flow, 

and intracellular streaming, may contribute to white matter anisotropy. The 

anisotropic nature of diffusion in the brain can be appreciated by comparing 

images obtained with DW gradients applied in three orthogonal directions. In each 

of the images, the signal intensity is equal to the signal intensity on echo-planar 

T2-weighted images decreased by an amount related to the rate of diffusion in the 

direction of the applied gradients. Images obtained with gradient pulses applied in 

one direction at a time are combined to create DW images or ADC maps. The 

ADC is actually a tensor quantity or a matrix: 

ADCxx ADCxy ADCxz 

ADC= [ ADCyx ADCyy ADCyz] 

ADCzx ADCzy ADCzz 

The diagonal elements of this matrix can be combined to give information about 

the magnitude of the apparent diffusion:

(ADCxx 1 ADCyy 1 ADCzz)/3 (Schaefer et al, 2000). 

- 40 - 


b value: 

The signal sensitivity to motion for the technique is determined by the b 

value. Larger b values can be obtained through larger gradient amplitudes, longer 

duration gradient pulses, or longer times between the gradient pulses. 

Increasing the b value will increase the amplitude of the diffusion gradients 

making the acquisition more sensitive to the diffusion of water in normal brain. As 

this occurs, the signal from areas with normal diffusion decreases, increasing the 

contrast between areas of normal and restricted diffusion (Westbrook , 1999). 

ADC map 

A parameter map in which the pixel intensity is equal to the value of ADC. 

The map may be obtained from images acquired at several different values of b- 

factor. Care must be taken in selecting a minimum b value as flow effects dominate 

at very low b. Alternatively, a two-point method may be used typically acquiring a 

b = 0 image and a second image at a high b value. ADC maps have proved useful 

in diagnosing stroke but do not provide any directional information (Liney, 2005). 

Motion artifact in DWI: 

All motion artifacts can produce false elevations in apparent diffusion 

coefficient values relative to the image in which b = 0. Patient motion, including 

gross head motion, cardiac related pulsations, and respiratory motions, can also 

produce large phase shifts, which create ghosting artifacts (Provenzale and 

Sorensen, 1999). 

With the development of fast imaging techniques such as single shot EPI 

and half Fourier RARE, it has been possible to suppress motion artifacts even with 

large diffusion gradients applied (Davis et al, 2003). 

MR Technique used for DWI 

With the development of high-performance gradients, DW imaging can be 

performed with an echo-planar spin echo T2-weighted sequence. With the original 

spin-echo T2-weighted sequence, even minor bulk patient motion was enough to 

obscure the much smaller molecular motion of diffusion. The substitution of an 

echo-planar spin-echo T2-weighted sequence markedly decreased imaging time

- 41 - 


and motion artifacts and increased sensitivity to signal changes due to molecular 

motion. As a result, the DW sequence became clinically feasible to perform 

(Schaefer et al, 2000). 

1) Ischemic Stroke 

The early diagnosis of ischemic stroke is critical to the success of 

therapeutic interventions such as thrombolysis and anticoagulation (Mullins, 

2006). 

Magnetic resonance (MR) diffusion imaging allows detection of cerebral 

ischemia within minutes of onset, and the temporal evolution of diffusion 

characteristics enables differentiation of acute from chronic stroke (Beaucbamp et 

al., 1998). 

Because diffusion-weighted MR imaging is especially sensitive to shifts in 

water that occur between extracellular and intracellular compartments, this 

technique can demonstrate regions of brain that are undergoing ischemic injury 

within 1 hour or less of symptom onset. In patients with acute ischemic stroke, 

intracellular swelling, which occurs as a result of water shifting from the 

extracellular compartment, causes the initial increase in observed signal intensity. 

Other factors that contribute to the increase in signal intensity are the 

increased tortuousity of the extracellular and intracellular spaces and increased 

intracellular viscosity (Chen et al, 2006). 

Conventional CT and MR imaging cannot reliably detect infarction at early 

time points (less than 6 h) (Gonzalez et al., 2006). In the hyperacute stroke period 

(0–6 hours after onset of symptoms), CT and MR imaging yield a sensitivity of 

less than 50% (Mullins et al, 2002), because detection of hypoattenuation on CT 

and hyperintensity on T2-weighted and fluid attenuated inversion recovery 

(FLAIR) MR images requires substantial increases in tissue water. For infarctions 

imaged within 6 h after stroke onset (Gonzalez et al., 2006). 

In contrast to CT and conventional MR imaging without diffusion 

weighting, DW imaging provides detection of lesions in the first hours after the 

onset of clinical symptoms. Furthermore, DW imaging is superior in detecting very 

small ischemic lesions due to the high signal intensity- to-noise ratio (Wessels et

al, 2005). 

- 42 - 


On ADC maps, tissues have an appearance opposite to that seen on the DWI 

trace. Thus, CSF is hyperintense on ADC maps, whereas on a DWI trace, CSF is 

hypointense. On diffusion-weighted images, lesions with restricted water diffusion 

are hyperintense while they are hypointense on ADC maps (Davis et al, 2003). 

In addition to Standard DW images and ADC maps, a third type of 

diffusion image can be created that combines some of the advantages of each. If 

one divides the DW image by the "b zero" reference image, or exponential image. 

Such an image is similar to standard DW scans, in that areas of acute ischemia 

appear hyperintense. Unlike standard DW images, however, so-called exponential 

images do not have any T2 weighting and thus do not show the effects of T2 shine- 

through (Haaga et al, 2003). 

Time course of Diffusion lesion evolution on acute stroke 

Information regarding the age of potentially salvageable tissue may be 

useful to establish rational time windows for stroke treatment and to identify 

patients who are most likely to benefit from acute stroke therapies. Second, 

knowledge of the natural evolution of MR characteristics may help estimate the 

age of a lesion when the time of symptom onset is unclear or when multiple lesions 

are present that could have different times of onset (Lansberg et al, 2001). 

In humans, decreased diffusion in ischemic brain tissue is observed as early 

as 30 min after vascular occlusion. The ADC continues to decrease with peak 

signal reduction at 1–4 days. This decreased diffusion is markedly hyperintense on 

DWI (a combination of T2 and diffusion weighting), less hyperintense on 

exponential images, and hypointense on ADC images. The ADC returns to 

baseline at 1–2 weeks. This is consistent with the persistence of cytotoxic edema 

(associated with decreased diffusion) as well as cell membrane disruption, and the 

development of vasogenic edema (associated with increased diffusion). At this 

point, a stroke is usually mildly hyperintense on the DWI images due to the T2 

component and isointense on the ADC and exponential images. Thereafter, the 

ADC is elevated secondary to increased extracellular water, tissue cavitation, and 

gliosis. There is slight hypointensity, isointensity or hyperintensity on the DWI

- 43 - 


images (depending on the strength of the T2 and diffusion components), increased 

signal intensity on ADC maps, and decreased signal on exponential images 


The time course is influenced by a number of factors including infarct type 

and patient age. Minimum ADC is reached more slowly and transition from 

decreasing to increasing ADC is later in lacunes versus other stroke types 

(nonlacunes). In nonlacunes, the subsequent rate of ADC increase is more rapid in 

younger versus older patients (Gonzalez et al., 2006). 

Although evolutions of infarction may differ according to the cerebral 

territories involved (Huang et al, 2001). Early reperfusion may also alter the time 

course .Early reperfusion causes pseudonormalization as early as 1–2 days in 

humans who receive intravenous recombinant tissue plasminogen activator (rtPA) 

within 3 hours after stroke onset (Gonzalez et al., 2006).

- 44 - 


Table 2: (Gonzalez et al., 2006) Diffusion MRI findings in stroke. (ADC Apparent 

diffusion coefficient, DWI diffusion-weighted image, EXP exponential image). 

Pulse 

sequance 

Reason for 

ADC 

changes 

DWI 

ADC 

EXP 

Hyperacute 

(0-6 h) 

Cytotoxic 

edema 

Hyperintense 

Hypointense 

Hyperintense 

Acute 

(6-24 h) 

Cytotoxic 

edema 

Hyperintense 

Hypointense 

Hyperintense 

Early 

subacute 

(1-7 days) 

Cytotoxic 

edema with 

small amount 

of vasogenic 

edema 

Hyperintense, 

gyral 

hypointensity 

from petechial 

hemorrhage 

Hypointense 

Hyperintense 

Late subacute Chronic 

Cytotoxic and 

vasogenic 

edema 

Hyperintense 

(due to T2 

component) 

Isointense 

Isointense 

vasogenic 

edema then 

gliosis and 

neuronal loss 

Isointense to 

hypointense 

Hyperintense 

Hypointense 

Diffusion-weighted (DW) imaging assesses the mobility of water. Severe 

cerebral hypoperfusion causes a restriction in the diffusion capacity of water due to 

cytotoxic edema and leads to an increased signal intensity on DW images. 

Increased signal intensity is also observed when the blood-brain barrier is 

disrupted. These two situations can be differentiated by calculating the apparent 

diffusion coefficient (ADC), a quantitative assessment of the diffusion capacity of 

water. When predominant cytotoxic edema is present, ADC levels are lower; by 

contrast, when the blood-brain barrier is disrupted, vasogenic edema develops, 

raising the ADC (Somford et al, 2004). 

Reversibility of DWI Stroke Lesions 

In the absence of thrombolysis, reversibility (abnormal on initial DWI but 

normal on follow-up images) of DWI hyperintense lesions is very rare (Gonzalez

et al., 2006). 

- 45 - 


Only few convincing cases had been reported in the literature with 

resolution of DWI lesions (mostly small lesions, often located in white matter) 

(Kummer and Back, 2006)The etiologies are acute stroke or transient ischemic 

attack (TIA), transient global amnesia, status epilepticus, hemiplegic migraine, and 

venous sinus thrombosis. ADC ratios (ipsilateral abnormal over contralateral 

normal-appearing brain) were similar to those in patients with acute stroke. In the 

setting of intravenous and/or intra-arterial Thrombolysis, DWI reversibility is more 

common. A number of studies have demonstrated that ADCs are significantly 

higher in DWI-reversible tissue compared with DWI-abnormal tissue that infarcts 


Reliability 

In contrast to unenhanced CT or conventional MR imaging, which have low 

sensitivities (50%) for acute ischemia detection within the first 6 hours after onset, 

diffusion-weighted imaging was reported to have had high sensitivity and 

specificity, of 88%–100% and 86%–100%, respectively, in various studies 

(Srinivasan et al, 2006). 

DWI can show small lesions adjacent to the cerebrospinal fluid. The 

diagnosis of a small cortical or brainstem infarct may be difficult on T2–WI 

images while DWI easily depicts such lesions. Fluid attenuated inversion recovery 

(FLAIR) demonstrates similar sensitivity to ischemic lesions than DWI, but does 

not allow demonstration of early lesions and differentiation between new and old 

lesions (Davis et al, 2003). 

Although after 24 h, CT, FLAIR and T2-weighted images are reliable at 

detecting acute infarctions, diffusion imaging continues to improve stroke 

diagnosis in the subacute setting. Older patients commonly have FLAIR and T2 

hyperintense white matter abnormalities that are indistinguishable from acute 

infarctions. However, the acute infarctions are hyperintense on DWI and 

hypointense on ADC maps while the chronic foci are usually isointense on DWI 

and hyperintense on ADC maps due to elevated diffusion (Gonzalez et al., 2006). 

DWI has proved to be more sensitive than CT in the assessment of the

- 46 - 


involved extent of the MCA territory. DWI and CT sensitivity ranges between 57% 

and 86% and 14% and 43%, respectively. Specificity has been reported excellent 

for both imaging techniques and interobserver agreement has shown only 

moderately good in both imaging techniques (kappa: 0.6 for DWI and 0.5 for CT) 

Furthermore, DWI has shown a more efficient early predictor of the volume of 

tissue ultimately infarcted than CT (Davis et al, 2003). 

Pitfalls of DWI in stroke: 

False negative DWI 

In the vertebro-basilar territory, there has been some concern about false- 

negative DWI studies,which have been reported in 19% to 31% of patients with 

stroke in the posterior circulation. The occurrence of false-negative DWI findings 

was significantly higher for small lesions and during the first 24 hours after stroke 

onset. In the anterior circulation, false negative initial DWI studies are much rarer 

(2%) (Davis et al, 2003). 

Most false-negative DWI images occur with punctuate lacunar brainstem or 

deep gray nuclei infarctions. Some lesions were presumed on the basis of an 

abnormal neurologic exam. While others were are seen on follow-up DWI. False 

negative DWI images also occur in patients with regions of decreased perfusion 

(increased mean transit time and decreased relative cerebral blood flow) that are 

hyperintense on follow-up DWI; that is, they initially had brain regions with 

ischemic but viable tissue that eventually infarcted. These findings stress the 

importance of obtaining early follow-up imaging in patients with normal DWI 

images and persistent stroke-like deficits so that appropriate treatment is initiated 

as early as possible (Gonzalez et al., 2006). 

False positive DWI 

False-positive DWI images occur in patients with a subacute or chronic 

infarction with “T2 shine through”. In other words, a lesion appears hyperintense 

on the DWI images due to an increase in the T2 signal rather than a decrease in 

diffusion. If the DW images are interpreted in combination with ADC maps or 

exponential images, this pitfall can be avoided. False-positive DWI images have

- 47 - 


also been reported with cerebral abscess (restricted diffusion due to increased 

viscosity), and tumor (restricted diffusion due to dense cell packing). Other entities 

with decreased diffusion that may be confused with acute infarction are venous 

infarctions, demyelinative lesions (decreased diffusion due to myelin 

vacuolization), hemorrhage and herpes encephalitis (decreased diffusion due to cell 

necrosis) .When these lesions are reviewed in combination with routine T1, 

FLAIR, T2, and gadolinium-enhanced T1-weighted images, they are usually 

readily differentiated from acute infarctions (Gonzalez et al., 2006). 

Artifacts on Diffusion –Weighted Images 

Acute stroke is characterized by high signal intensity on DW images; 

however, there are other causes of high signal intensity on these images. Knowing 

these other causes can be helpful in assessing the likelihood that a given patient has 

evidence of cerebral ischemia. 

One commonly seen artifact that can mimic the appearance of acute stroke 

is known as T2 shine-through .Because DW scans also typically have substantial 

spin density and T2 weighting, areas of T2 prolongation may result in carryover of 

hyperintense signal to the DW image. Careful comparison with a reference image 

(i.e., the "b zero" image) or another type of T2-weighted image can be helpful in 

recognizing this artifact. 

Another artifact that can mimic the appearance of acute stroke on DW 

images is hyperintensity due to white matter diffusion anisotropy. If one reviews 

DW images that have been sensitized to diffusion in only one direction (e.g., the 

phase-encoding direction), the white matter tracts that run orthogonal to the 

direction of sensitization appear relatively bright. This artifact can be recognized 

with experience, although comparison with DW images obtained with the diffusion 

–sensitizing gradients applied in other directions can be helpful. One can eliminate 

this artifact completely by reviewing only images that have isotropic weighting. 

Another artifactual cause of hyperintense signal on DW scans is related to 

magnetic susceptibility artifacts. Most DW scans are made using echo-planer 

imaging techniques. These very rapid MRI methods are commonly used for DW 

images because DW scans are highly sensitive to patient motion.

- 48 - 


One potential problem with echo-planar images is that they are very 

sensitive to susceptibility artifacts at soft tissue/ bone and soft tissue/ air interfaces 

.Foreign bodies (e.g., shunt catheters) may also produce susceptibility artifacts are 

usually easy to recognize because: 

They occur in locations (e.g., calvarium and skull base) that are prone to such 

artifacts. 

1- They are often flame-shaped. 

2- When sever, they can cause regional anatomic distortion in addition to 

causing increased signal intensity (Haaga et al, 2003). 

Stroke Mimics 

These syndromes generally fall into four categories: (1) Non ischemic 

lesions with no acute abnormality on routine or diffusion-weighted images; (2) 

ischemic lesions with reversible clinical deficits which may have imaging 

abnormalities; (3) Vasogenic edema syndromes which may mimic acute infarction 

clinically and on conventional imaging; (4) other entities with decreased diffusion 

patients (Gonzalez et al., 2006). 

Non ischemic Lesions with No Acute Abnormality on Routine or Diffusion- 

Weighted Images 

Non ischemic syndromes that present with signs and symptoms of acute 

stroke but have no acute abnormality identified on DWI or routine MR images 

include peripheral vertigo, migraines, seizures, dementia, functional disorders, and 

metabolic disorders. The clinical deficits associated with these syndromes are 

usually reversible. If initial imaging is normal and a clinical deficit persists, repeat 

DWI should be obtained. False-negative DWI and perfusion weighted images 

(PWI) occur in patients with small brainstem or deep gray nuclei lacunar 

infarctions patients (Gonzalez et al., 2006). 

Syndromes with Reversible Clinical Deficits that may have Decreased 

Diffusion 

Transient Ischemic Attack 

A transient ischemic attack (TIA) can be defined as a sudden loss of

- 49 - 


neurological function lasting less than 24 hours due to occlusive thromboembolic 

cerebrovascular disease (Crisostomo et al, 2003). 

DWI demonstrates ischemic abnormalities in nearly half of clinically 

defined TIA patients. The lesions are usually less than 15mm in maximal diameter. 

The percentage of patients with positive DWI lesion increases with increasing total 

symptom duration. The compromised vascular territory detected on diffusion 

imaging and the clinical symptoms correlate. In nearly half the patients the 

diffusion MRI changes may be fully reversible, while in the remainder the findings 

herald the development of a parenchymal infarct (Kesavadas et al., 2003). 

Transient Global Amnesia 

Transient global amnesia (TGA) is a clinical syndrome characterized by 

sudden onset of profound memory impairment resulting in both retrograde and 

anterograde amnesia without other neurological deficits. The symptoms typically 

resolve in 3–4 h. Many patients with TGA have no acute abnormality on 

conventional or diffusion-weighted images .A number of studies, however, have 

reported punctuate lesions with decreased diffusion in the medial hippocampus, the 

parahippocampal gyrus, and the splenium of the corpus callosum (Gonzalez et al., 

2006). 

Vasogenic Edema Syndromes 

Patients with these syndromes frequently present with acute neurologic 

deficits, which raise the question of acute ischemic stroke. Furthermore, 

conventional imaging cannot reliably differentiate cytotoxic from vasogenic edema 

because both types of edema produce T2 hyperintensity in gray and/or white 

matter. Diffusion MR imaging has become essential in differentiating these 

syndromes from acute stroke because it can reliably distinguish vasogenic from 

cytotoxic edema. While cytotoxic edema is characterized by decreased diffusion, 

vasogenic edema is characterized by elevated diffusion due to a relative increase in 

water in the extracellular compartment. Vasogenic edema is characteristically 

hypointense to slightly hyperintense on DWI images because these images have 

both T2 and diffusion contributions . Vasogenic edema is hyperintense on ADC 

maps and hypointense on exponential images while cytotoxic edema is

- 50 - 


hypointense in ADC maps and hyperintense on exponential images patients 


Venous Infarction 

Cerebral venous sinus thrombosis (CVT) is a rare condition that affects 

fewer than 1 in 10,000 people. The pathophysiology of CVT is not completely 

clear. Venous obstruction results in increased venous pressure, increased 

intracranial pressure, decreased perfusion pressure, and decreased cerebral blood 

flow. Increased venous pressure may result in vasogenic edema from breakdown of 

the blood–brain barrier and extravasation of fluid into the extracellular space. 

Blood may also extravasate into the extracellular space. Severely decreased blood 

flow may also result in cytotoxic edema associated with infarction. Increases in 

CSF production and resorption have also been reported. Parenchymal findings on 

imaging correlate with the degree of venous pressure elevation .With mild to 

moderate pressure elevations, there is parenchymal swelling with sulcal effacement 

but without signal abnormality. As pressure elevations become more severe, there 

is increasing edema and development of intraparenchymal hemorrhage. Superior 

sagittal sinus thrombosis is characterized by bilateral parasagittal T2-hyperintense 

lesions involving cortex and subcortical white matter. Transverse sinus thrombosis 

results in T2-hyperintense signal abnormality involving temporal cortex and 

subcortical white matter. Deep venous thrombosis is characterized by T2- 

hyperintense signal abnormalities in the bilateral thalami and sometimes the basal 

ganglia. Hemorrhage is seen in up to 40% of patients with CVT and is usually 

located at gray white matter junctions or within the white matter. 

DWI has proven helpful in the differentiation of venous from arterial 

infarction and in the prediction of tissue outcome. T2-hyperintense lesions may 

have decreased diffusion, elevated diffusion or a mixed pattern. Lesions with 

elevated diffusion are thought to represent vasogenic edema and usually resolve. 

Lesions with decreased diffusion are thought to represent cytotoxic edema. Unlike 

arterial stroke, some of these lesions resolve and some persist. Resolution of 

lesions with decreased diffusion may be related to better drainage of blood through 

collateral pathways in some patients (Gonzalez et al., 2006).

- 51 - 


- 52 - 


2) Hemorrhagic Stroke 

- 53 - 


Intraparenchymal Hemorrhage: Appearance and Evolution 

The classic pattern for temporal evolution of intracerebral hematomas on 

MRI at1.5 T is well known. However, determination of the age of hemorrhage is 

often inaccurate because of variations between individual patients. The change of 

signal intensity over time depends on many factors, such as the oxygenation state 

of hemoglobin, the status of red blood cell membrane, hematocrite, proteins and 

clot formation. Among these, the evolution of hemoglobin and red cell membrane 

integrity are most important. The transition of oxy-hemoglobin to deoxy- 

hemoglobinand thereafter to met-hemoglobin depends primarily upon oxygen 

tension in the vicinity of the lesion as well as inside the hematoma itself. In the 

hyperacute stage, oxy-hemoglobin will dominate initially, but transformation into 

deoxy-hemoglobin will soon take place and deoxy-hemoglobin will dominate after 

a few days- the acute hematoma. After approximately one week, deoxy 

hemoglobin will transform to met-hemoglobin. However, the rate of this oxidation 

to met-hemoglobin will depend on oxygen tension in the tissues, which may 

further complicate the temporal pattern of expected signal changes. Initially, met- 

hemoglobin will be found within intact red blood cells ( the early subacute stage), 

but when the red cell membrane start to rupture, met-hemoglobin will be found in 

the extracellular fluid space ( The late subacute stage) , which takes place about 

two weeks following hemorrhage. The final stage, the chronic stage, is the result of 

continous phagocytation of the breakdown products of hemoglobin, ferritin and 

hemosiderin, which starts about one month following hemorrhage. The products 

ferritin and hemosiderin, will remain within the phagocytic cells, which 

accumulate in the periphery of the hematoma, where they may remain for years, 

may be indefinitely, as a marker of an old hemorrhage (Moritani et al, 2005). 

Diffusion MR data would differ among the stages of evolving hematomas in 

that hematomas containing blood with intact cell membranes would have restricted 

diffusion compared with those hematomas in which RBC membranes have lysed. 

This hypothesis was based on several facts. First, the presence of intact cell

- 54 - 


membranes restricts molecular diffusion .For instance, increased ADC values have 

been reported in cases of intratumoral necrosis, a pathologic environment defined 

by a lack of intact cell membranes. Second, an important requisite for the diffusion 

restriction observed in association with early ischemic infarction is the presence of 

intact cells, because the early reduction in diffusion is related to shifts of water 

from extracellular space to intracellular space. Once cells have lysed in the 

subsequent evolution of subacute to chronic infarction, measured diffusion 

increases. Hematomas composed of any and all of the evolutionary stages 

theorized to contain hemoglobin within intact RBCs (i.e., hyperacute, acute, and 

early subacute hematomas) show significantly reduced ADC values compared with 

the single hematoma state theorized to be comprised of lysed RBCs (i.e., ‘‘free’’ 

methemoglobin in subacute-to-chronic hematomas). The ADC measurements in all 

of the intracellular hemoglobin states (intracellular oxyhemoglobin, intracellular 

deoxyhemoglobin, and intracellular methemoglobin) were statistically equivalent. 

These diffusion data support the theorized biophysical states of hemoglobin and 

the RBC put forth in the literature on evolving intracranial hematomas. Further 

analysis indicated that the ADC measurements of all early hematomas (including 

hyperacute, acute, and even early subacute) were significantly reduced compared 

with normal brain tissue. This restriction of diffusion is similar to the phenomenon 

observed in cases of early ischemic infarction, in which it is well documented that 

within minutes and for the first several days, the ADC value decreases and is 

therefore depicted as marked hypointensity on ADC maps. The precise biophysical 

explanation for the observed restriction of diffusion in early stages of intracranial 

hematomas is uncertain. Potential causes include, but are not limited to: 1) 

Shrinkage of extracellular space with clot retraction 2) a change in the osmotic 

environment once blood becomes extravascular, which alters the shape of the RBC 

-a phenomenon related to the formation of the fibrin network associated with clot 

3) a conformational change of the hemoglobin macromolecule within the RBC ; 

and the less likely possibility of 4) contraction of intact RBCs (thereby decreasing 

intracellular space) Any of these processes might alter the potential mobility of 

intracellular water protons. Regardless of the precise explanation for restricted

- 55 - 


diffusion in early hematomas, our study indicates that the measured restriction of 

diffusion (reduced ADC value) in the hematoma itself would generate similar 

hypointensity on ADC maps (Atlas et al, 2000) 

Hyperacute Hematoma 

Results of DW imaging of hematomas at this stage have not been well 

characterized; however a hyperacute intraparenchymal hemorrhage is hyperintense 

on DW images, with a decreased apparent diffusion coefficient (ADC). The 

possible causes for the decreased ADC are shrinkage of the extracellular space due 

to clot retraction, changes in the concentration of hemoglobin and a high viscosity 

(Moritani et al, 2005). 

Acute hematoma 

Diffusion-weighted images of an acute hematoma show a marked 

hypointensity, caused by the magnetic field inhomogeneity created by the para- 

magnetic deoxy-hemoglobin. Although The ADC has been reported to be 

decreased, accurate calculations are often difficult (Moritani et al, 2005). 

Early subacute hematoma 

On DW imaging, intracellular met-hemoglobin shows hypointensity due to 

paramagnetic susceptibility effects and ADC measurements are not reliable due to 

susceptibility effects (Moritani et al, 2005). 

Late subacute hematoma 

It has been reported that late subacute hematomas are hyperintense on DW 

imaging. The ADC value for the late subacute hematoma is controversial 


Chronic hematoma 

Diffusion-weighted images are hyperintense in chronic hematomas. The 

ADC value has been reported to be increased, but this is often difficult to measure 

accurately due to paramagnetic susceptibility artifacts (Moritani et al, 2005) 

Hemorrhagic and Non hemorrhagic Stroke 

(a) Decreased ADC was demonstrated in the lesions of acute hemorrhagic 

stroke and in the lesions of acute non hemorrhagic stroke; (b) acute hemorrhagic

- 56 - 


stroke was depicted as an area of hypointensity on T2-weighted EP images, in 

contrast to the normal to increased signal intensity in lesions of acute non 

hemorrhagic stroke; and (c) decreased ADC tended to persist longer in 

hemorrhagic stroke lesions than in non hemorrhagic stroke lesions (Ebisu et al, 

1997). 

Restriction of diffusion, even in the appropriate clinical setting of acute 

stroke by clinical assessment, should not necessarily be taken as specific for acute 

ischemic infarction. Second, several studies quantify regions of acute infarction on 

the basis of restricted diffusion on ADC maps. A potential pitfall to that 

quantitative assessment in that early hematomas might mask or mimic regions of 

acute infarction. This suggests that ADC maps should always be interpreted with 

conventional MR images for comparison (Atlas et al, 2000). 

Subarachnoid hemorrhage 

Computed tomography (CT) is still essential in the diagnosis of acute 

subarachnoid hemorrhages, as the sensitivity and usefulness of MR imaging is 

controversial. Fluid –attenuated inversion-recovery (FLAIR) imaging has a high 

sensitivity for subarachnoid hemorrhage.However, the sensitivity is low. 

It is often difficult to detect subarachnoid hemorrhage on DW images. 

However, DW images may be useful to visualize parenchymal injuries secondary 

to subarachnoid hemorrhage. Ischemic changes, probably related to subarachnoid 

hemorrhage, have showen hyperintensity on DW images (Moritani et al, 2005). 

Intraventricular Hemorrhage 

Intraventricular hemorrhage is well demonstrated on FLAIR, T1, T2 and 

proton density-weighted images. FLAIR has been reported to have highest 

sensitivity for detection of intraventricular hematomas. DW images can 

demonstrate intraventricular hemorrhages, but in general the GRE images have a 

higher sensitivity (Moritani et al, 2005).

- 57 - 


- 58 - 


- 59 - 


- 60 - 


Perfusion is the steady-state delivery of blood (nutrients and oxygen) to 

tissue parenchyma representing coherent motion of water and cellular material. 

Since both perfusion-weighted imaging (PWI) and magnetic resonance 

angiography (MRA) map the flow of blood in vessels, there may be some 

confusion between the applications of these two techniques. MRA is useful in 

demonstrating the macroscopic vasculature (in both arteries and veins) and 

detecting morphological changes in blood vessels themselves such as stenosis, 

aneurysms, dissections and malformations. PWI detects microscopic flow at the 

capillary level and therefore is useful to investigate changes taking place at the 

cellular level (Davis et al, 2003). 

Perfusion is typically measured in ml/100gm of tissue /min, or units of 

CBF. Normal human gray matter is perfused at a rate of 50-60ml/100gm/min and 

is maintained in a narrow range by cerebral auto-regulation .Thus, low perfusion 

states might result in cellular ischemia, and high perfusion states might be 

associated with hypervascular lesions such as some tumors (Sorensen and Reimer, 

2000). 

Clinical Application of Perfusion Weighted 

There are three important parameters that are used to quantify and assess 

brain tissue perfusion: cerebral blood flow (CBF), cerebral blood volume (CBV) 

and mean transit time (MTT). CBV is defined simply as the amount of blood in a 

given amount of tissue at any time (ml/g) as compared to CBF, which represents 

the amount of blood moving through a certain amount of tissue per unit time (ml/g 

per min). The ratio of CBV and CBF is defined as the mean transit time (units 

minutes) (Davis et al, 2003). 

Imaging in Stroke 

Perfusion imaging techniques can be divided into two broad groups, 

depending upon the type of contrast mechanism: 

(i) signal monitoring using exogenous (injectable) contrast agents such as

- 61 - 


gadolinium DTPA (Gd-DTPA; T1 shortening agent), oxygen 17 in H2O17 (T2 

shortening agent) or superparamagnetic agents (T2* shortening). 

(ii) Endogenous or inherent contrast agents such as arterial spin labelling 

technique (ASL) (Davis et al, 2003).The target of acute stroke therapy is that 

portion of the brain tissue that is ischemic and contributes to the neurologic deficit 

but is still viable and salvageable if appropriate blood flow is rapidly restored 

(Grandian et al, 2002). 

Viable tissue that is at risk for infarction is commonly called the ischemic 

penumbra or the tissue outside the (non viable) core of infarction that is 

nonetheless under perfused. It is postulated that the ischemic penumbra differs 

from viable tissue that is not at risk by the (decreased) amount of blood flow that it 

receives (Haaga et al, 2003). 

Depending on the effectiveness of collateral vessels, such tissue may persist 

as long as 17 hours after stroke onset in some patients or, inversely, may be 

irreversibly damaged within a few minutes after the arterial occlusion . Therefore, 

thrombolytic therapy should be individually tailored (Grandian et al, 2002). 


irreversibly infarcted tissue (Srinivasan et al, 2006), perfusion imaging findings 

provide information on the momentary hemodynamic state of brain tissue, as they 

reveal impaired tissue perfusion caused by blood vessel obstruction. Therefore, 

perfusion imaging findings may yield information about pathologically 

hypoperfused regions, even before genuine structural brain tissue damage has 

taken place (Wittsack et al, 2002). 

The pathophysiology of ischemia can be considered in four stages, based on 

autoregulatory physiology: 

First stage, normal hemodynamics. 

Second stage, characterized by initial decrease in perfusion pressure. Initially, 

autoregulatory vasodilatation preserves CBF, at the same time increasing CBV. 

MTT is also typically increased. 

Third stage, characterized by greater decrease in perfusion pressure and by an 

initial decrease in CBF value. CBV typically remains increased.

- 62 - 


Fourth stage, characterized by further decrease in perfusion pressure and decrease 

in both CBF and CBV. This stage is associated with tissue ischemia and 

hemodynamic failure (Haaga et al, 2003). 

Reduced rCBF represents ischemic threat to brain tissue, increased rMTT 

represents the brain’s active response to that threat, and reduced rCBV may 

represent failure of that response to meet metabolic needs. In this view, regions of 

reduced rCBV represent tissue that is very likely destined for infarction, but 

regions of abnormal rCBF or rMTT may or may not proceed to infarction (Davis et 

al, 2003). 

Reliability 

In general, perfusion images are less sensitive than DWI images in the 

detection of acute stroke. Lesions missed on perfusion images include: (1) lesions 

with small abnormalities on DWI that are not detected because of the lower 

resolution of MR perfusion images, and (2) lesions with early reperfusion. 

Specificities for perfusion images range from 96% to 100%. Occasional false- 

positive scans occur when there is an ischemic, but viable hypoperfused region that 

recovers (Gonzalez et al., 2006). 

It has been proposed that MR perfusion imaging may complement DW 

imaging in depicting the region of penumbra. The premise is that DW imaging is 

thought to depict the region of core infarction, whereas the region of perfusion 

abnormality represents both the core and the penumbra. The difference between 

the extent of the diffusion abnormality and the extent of perfusion abnormality is 

thus thought to represent penumbra (Haaga et al, 2003). 

Addition of perfusion to diffusion information increases the sensitivity for 

detecting ischemic at-risk tissue and categorizing its vascular distribution to enable 

the best selection among therapeutic options. (Sunshine et al, 2001). 

Until now, recanalization treatment with using thrombolytics has been the 

only effective treatment for hyperacute ischemic stroke. The procedure is usually 

done within three hours after the onset of symptoms for the intravenous method, 

and it’s done within six hours for the intraarterial method. This quick intervention 

is based upon the hypothesis that there is a significant portion of tissue at risk of

- 63 - 


irreversible injury that could be recovered if swift reperfusion is within these time 

periods. The area that can be salvaged by timely reperfusion is referred to as the 

“ischemic penumbra.” The aim of radiological imaging before recanalization 

treatment is to identify those patients who can most benefit from the treatment and 

to exclude those patients who are at a large degree of risk with using recanalization 

treatment (Lee et al., 2005). 

Proximal occlusions are much more likely to result in a diffusion–perfusion 

mismatch than distal or lacunar infarctions. Operationally, the diffusion 

abnormality is thought to represent the ischemic core and the region characterized 

by normal diffusion but abnormal perfusion is thought to represent the ischemic 

penumbra. Definition of the penumbra is complicated because of the multiple 

hemodynamic parameters that may be calculated from the perfusion MRI data 


The volume of penumbral tissue typically decreases with time as the infarct 

expands, but the duration of the potential therapeutic window is variable (Prosser 

et al, 2005).

- 64 - 


Table 3: (Gonzalez et al., 2006) Lesion volumes of diffusion and perfusion. (DWI 

Diffusion-weighted imaging, PWI perfusion-weighted imaging). 

Pattern Cause Comment 

PWI but no DWI 

PWI>DWI 

PWI=DWI 

PWI

- 65 - 


A diffusion lesion larger than the perfusion lesion or a diffusion lesion without a 

perfusion abnormality usually occurs with early reperfusion. Similarly, in this 

situation, there is usually no significant lesion growth (Gonzalez et al., 2006). 

An alternate approach for determining the extent of penumbra is to use 

perfusion maps alone to distinguish the core of infarction from the penumbra. 

Usually with the use of perfusion parameter value thresholds. The most commonly 

used perfusion parameter is the mean CBF value (Haaga et al, 2003). 

The variability in CBF ratios likely results from a number of different 

factors. Most importantly, the data obtained represent only a single time point in a 

dynamic process. One major factor is variability in timing of tissue reperfusion. 

Another factor is that normal average CBF in human parenchyma varies greatly, 

from 21.1 to 65.3 ml .100 g –1 .min –1 ,depending on age and location in gray matter 

versus white matter. Other factors affecting thresholds of tissue viability include 

variability methodologies, variability in initial and follow-up imaging times, and 

variability in post ischemic tissue responses. 

Low rCBV ratios are highly predictive of infarction. However, elevated 

rCBV is not predictive of tissue viability, and rCBV ratios for penumbral regions 

that do and do not infarct may not be significantly different. Some studies have 

demonstrated no statistically significant differences in MTT between infarct core 

and the two (viable and nonviable) penumbral regions, while others have 

demonstrated differences between all three regions or between the viable and 

nonviable penumbral regions. (Gonzalez et al., 2006). 

Correlation of Diffusion and Perfusion MRI with Clinical Outcome 

Attempts have been made to combine DWI and PWI by comparing lesion 

volumes identified by the 2 techniques. Diffusion-perfusion mismatches,” in which 

the lesion volumes identified by one modality are larger than those by the other, 

have been reported by several groups. Larger lesion enlargement of the acute DWI 

lesion volume in cases where the acute PWI volume is larger than the DWI lesion. 

In cases where the acute DWI lesion was larger than the PWI lesion, total lesion 

growth was reduced. Based on these observations, many have hypothesized that 

these DWI-PWI mismatches may allow identification of salvageable tissue in

individual patients (Wu et al, 2001). 

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Now that thrombolytic therapy is commonly employed in acute stroke 

management, predicting the extent to which acute infarcts will grow in the days 

following presentation is increasingly important. Intravenous or intra-arterial 

thrombolysis is capable of saving substantial quantities of brain tissue that 

otherwise would have undergone infarction, resulting in marked reduction of 

permanent neurologic deficits. However, thrombolysis also carries considerable 

risk of catastrophic intracranial hemorrhage. The decision of whether or not to 

accept this risk and proceed with thrombolysis is a highly individualized one. In 

making that decision, clinicians, patients and their families would benefit from an 

informed estimation of how much brain tissue will be affected, and how severe 

neurological deficits are likely to be, if thrombolytic therapy is not initiated (Davis 

et al, 2003). 

Diffusion and perfusion MRI in predicting clinical outcome (Gonzalez et al., 

2006) 

1. DWI, CBV, CBF, MTT, and TTP initial lesion volumes all correlate with acute and chronic 

neurologic assessment tests. It’s unclear which parameter is best. 

2. DWI initial lesion volume correlation with outcome scales is higher for cortical than for 

penetrator artery strokes. 

3. Patients with a mismatch (proximal stroke) usually have worse clinical outcomes compared 

to patients without a mismatch (distal or lacunar stroke). 

4. Size of the diffusion–perfusion mismatch volume correlates with clinical outcome. 

5. Amount of decrease in size of MTT abnormality volume following intravenous 

thrombolysis correlates with clinical outcome.

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- 68 - 


One of the strengths of MRI for imaging patient tissue is its ability to 

acquire information regarding its function as well as its structure. The most 

common example is the examination of flowing blood within the vascular network 

using MR angiography (MRA). Moving tissue was shown to produce severe image 

artifacts. MRA uses flowing tissue such as blood to provide the primary source of 

signal intensity in the image. It provides visualization of the normal, laminar flow 

of blood within the vascular system and its disruptions due to pathologic 

conditions such as stenoses or occlusions. MRA can be of particular benefit in 

evaluating vessel patency. MRA techniques have the advantage over conventional 

X-ray-based angiographic techniques in that use of a contrast agent is not always 

required. Consequently, multiple scans may be performed if desired (e.g., 

visualizing arterial then venous flow) (Brown and Semelka, 2003). 

Magnetic resonance angiography (MRA) is a set of vascular imaging 

techniques capable of depicting the extracranial and intracranial circulation. In the 

setting of acute stroke, these techniques are useful for determining stroke etiology 

and assessing vascular flow dynamics. Specifically, they are used to evaluate the 

severity of stenosis or occlusion as well as collateral flow. A typical stroke 

protocol includes two-dimensional (2D) and/or three-dimensional (3D) time of- 

flight (TOF) and contrast-enhanced MRA images through the neck and 3D TOF 

MRA images through the Circle of Willis (Gonzalez et al., 2006). 

MRA is broadly divided into non contrast and contrast-enhanced 

techniques. Non contrast MRA can be acquired with phase contrast (PC) or TOF 

techniques, and both can be acquired as 2D slabs or 3D volumes (Gonzalez et al., 

2006). 

Clinical Application of MRA in Stroke 

Magnetic resonance angiography (MRA) uses the inherent motion 

sensitivity of MRI to visualize blood flow within vessels. There are two major 

classes of flow imaging methods that rely on the endogenous contrast of moving 

spins to produce angiographic images.

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The time-of-flight (TOF) technique relies on flow dependent changes in 

longitudinal magnetization, whilst the phase-contrast (PC) technique relies on flow 

dependent changes in transverse magnetization. In addition there are contrast- 

enhanced MRA techniques that employ exogenous contrast agents, such as 

gadolinium chelates, to provide vascular contrast (McRobbie et al., 2006). 

MR angiography has recently been established as a valid and sensitive tool 

to demonstrate pathologic findings in extra- and intracranial arteries in acute stroke 

(Seitz et al, 2005). 

Extracranial Steno-occlusive diseases 

MRA of neck vessels is important in stroke management because 

extracranial atherosclerosis causes an estimated 20–30% of strokes (Gonzalez et 

al., 2006). 

Intracranial Steno-occlusive diseases 

In setting of acute stroke, information about the status of the intracranial 

arteries is critical to determination of stroke subtype and associated prognosis, and 

helps to determine the choice to employ thrombolytic therapy (Davis et al, 2003). 

In the setting of acute stroke, intracranial MRA can detect areas of stenosis 

and occlusion as well as determine collateral flow. Defining the location of 

intracranial vessel pathology is clinically important since an estimated 38% of 

patients with acute strokes have arterial occlusion seen on DSA (Gonzalez et al., 

2006). 

The depiction of intracranial arterial stenosis by MRA requires a high 

sensitivity resolution technique, while the importance of an exact grading by MRA 

is not defined yet (Kummer and Back, 2006). 

Several studies report that intracranial MRA has a variable reliability of 

detecting occlusion and stenoses in the acute stroke setting (Gonzalez et al., 2006). 

In the diagnosis of intracranial stenosis, TOF MRA is definitely superior to 

PC-MRA protocols. Despite high anatomical resolution TOF-MRA does not allow 

an authentic quantification of intracranial vessel stenoses. Stenoses are commonly 

overestimated, especially in small vessels. Turbulences and velocity displacement

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effects depending on flow velocity and the tortuosity of a vessel cause false 

positive stenoses. Typical localizations of pseudostenoses are the carotid siphon 

and the bent entrance into the carotid canal. In CE-MRA the contrast medium 

limits spin saturation effects and very short echo times reduce the negative signal 

effect of turbulent flow patterns, whereby false positive intracranial stenosis can be 

identified. Currently, the spatial resolution of CE-MRA as obtained with sufficient 

signal-to-noise ratio and without relevant venous contrast overlap in the limited 

acquisition time is still significantly lower than that of TOF-MRA. Therefore, CE- 

MRA should be used intracranially as an add-on and not as a substitute for TOF- 

MRA (Kummer and Back, 2006). 

Time of flight MRA also has limitations. Whereas spatial resolution is 

adequate for the primary branches of the Circle of Willis, it is less so in the more 

distal, smaller branches and the level of diagnostic confidence diminishes (Davis et 

al, 2003). 

The degree of collateral flow seen on DSA is an independent radiologic 

predictor of favorable outcome following thrombolytic treatment. TOF MRA, 

however, is limited in evaluation of collateral flow (Gonzalez et al., 2006). 

A dedicated analysis of collateral circulations, especially extra- 

intracranially, is still the domain of DSA as far as the exact depiction of anatomical 

connections is of importance. If the exact anastomotic vascular anatomy is not of 

primary interest, the collateral supply is better determined by MR perfusion 

techniques Kummer and Back, 2006). 

Arterial Dissection 

Vascular dissection is an important etiology of acute infarction, causing up 

to 20% of infarcts in young patients and an estimated 2.5% of infarcts in the 

overall population (Gonzalez et al., 2006). 

Dissections occur post-traumatically or spontaneously, in conjunction with 

hypertension or with migraine, often with fibromuscular dysplasia or with other 

connective tissue diseases (Kummer and Back, 2006). 

MRI reveals a crescentic intramural hyperintensity on both T1- and T2- 

weighted images (Davis et al, 2003).Acute dissections show luminal narrowing on

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MRA and a flap can occasionally appear as a linear low signal defect on MRA 


Aneurysm 

Both MRA and CTA have been reported to be accurate tests for intracranial 

aneurysms, although the sensitivity diminishes greatly for smaller lesions. MRA is 

not a complete replacement for X-ray angiography. The accuracy of MRA might 

be sufficient to screen patients who are at risk for intracranial aneurysms (Davis et 

al, 2003). 

Vascular malformation 

MRI depicts the nidus of a vascular malformation, whereas MRA depicts 

the feeding arteries and draining veins. However, image quality is not sufficient to 

obviate the need for selective X-ray angiography prior to intervention. Contrast 

enhanced 3D MRA should provide more complete evaluation. When compared 

with DSA, the authors reported that CE 3DMRA consistently depicted AVM 

components and their orientation (Davis et al, 2003). 

Moya Moya 

The term moya moya refers to primary moya moya disease and moya moya 

pattern, associated with an underlying disease such as atherosclerosis or radiation 

therapy. There is an increased incidence of primary moya moya disease in Asians 

and in patients with neurofibromatosis or sickle cell disease. Pathologically, there 

is a progressive occlusive vasculopathy of the supraclinoid internal carotid artery 

with extension into the proximal anterior and middle cerebral arteries associated 

with characteristic dilated prominent collateral vessels. Pediatric patients with 

moya moya disease tend to develop symptoms from acute infarction while adults 

with moya moya disease more frequently present with symptoms from intracranial 

hemorrhage into the deep gray nuclei. MRA can depict stenoses and occlusion of 

the internal carotid, middle cerebral, and anterior cerebral arteries (Gonzalez et al., 

2006). 

Vasculitis 

Patients with vasculitis develop ischemic and thrombotic infarctions. There

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is also altered wall competence, which can result in dissection or vessel wall 

disruption with intracranial hemorrhage. MRA is clinically used to screen for 

vasculitis, but is less sensitive than DSA (Gonzalez et al., 2006) 

Although for a long time DSA was accepted as a diagnostic gold standard, 

MRI and MRA obviously provide the advantage not only to depict stenoses, but 

also to provide signs of inflammatory vessel disease. This provides new criteria for 

therapy monitoring. An appropriate examination consists of a CE-MRA, as well as 

acquisition of spin echo images (Kummer and Back, 2006). 

Fibromuscular Dysplasia 

Fibromuscular dysplasia (FMD) is a disease of medium-sized vessels, 

beginning in young to middle-aged patients with predominance among females 

(Kummer and Back, 2006). 

Fibromuscular dysplasia (FMD) is an uncommon idiopathic vasculopathy 

causing stenoses most often in the renal and internal carotid arteries, and patients 

with FMD of the neck vessels can present with infarcts or transient ischemic 

attacks (Gonzalez et al., 2006). 

FMD manifests through dissections or hyperplasia of the vessel walls with 

resulting stenosis. Stenosis and dilations with thinning of vascular walls alternate 

over longer distances, occasionally with aneurysms or luminal duplications. On 

DSA, this type of lesions was described as “string of beads”. The carotid artery is 

often affected bilaterally, mostly sparing the bifurcation. There is an elevated 

incidence of intracranial aneurysms and additionally arteriovenous fistulae can 

occur. 

MRA can provide evidence of dissections with high sensitivity and of 

alternating arterial dilatation and stenosed vessels. MRA may also to help identify 

the string of beads pattern. In source images of TOF-MRA, segmental changes in 

arterial wall thickness, however, are detected to only a limited extent (Kummer 

and Back, 2006).

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- 74 - 


- 75 - 


MR spectroscopy enables non-invasive in vivo study of some phases of 

brain metabolism. It is based on the same principles as conventional MR, except 

that it envisages signal processing during and after sequence acquisition. Whereas 

in standard MR the signal intensity is the sum of the signals from all the hydrogen- 

containing molecules in a given volume, in spectroscopy the signal from a given 

nucleus is separated into its chemical components (Salvolini and Scarabino, 

2006). 

Clinical Application of MRS in Stroke 

The techniques used most often in clinical practice, are proton spectroscopy 

(1H MRS) and phosphor spectroscopy (3IP MRS)-those nuclei play the crucial role 

in metabolic turn over. The first gives information about various metabolic 

disorders (acethyl-aspartate acid- nervous cells marker, creatinin- related to 

metabolic changes, choline- element of cell membranes, lactates- markers of 

anaerobic metabolism). The second enables evaluation of energetic condition of 

the cells (phosphate compounds, mono-and biphosphate, phosphor-creatinin, 

adenosine triphosphate ATP) (Kaminska et al, 2007). 

However, not all metabolites contain phosphorus, and the MR application of 

this nucleus has been restricted to the study of energy and lipid metabolism. In the 

brain, [1H]-MRS has two great advantages: the proton provides 15 times more 

sensitivity than [31P]-MRS and almost every compound in living tissue contain 

hydrogen (Davis et al, 2003). 

Single Voxel Spectroscopy 

The practical use of in vivo MRS requires a method, which enables 

registering the spectrum of selected volume, called the "volume of interest" (VOI) 

or voxel. 

Multi- Voxel Spectroscopy (Chemical Shift Imaging-CSI) 

The CSI technique, which visualizes the chemical shift in one measurement 

period, it collects spectroscopic signals from multiple small voxels located within a 

large examined area. The registered signals form a map of spatial distribution of

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the metabolites. The signals from particular voxels can be shown as spectra and 

further analyzed, like in the SVS (Kaminska et al, 2007). 

The normal [1H]-MRS spectrum 

Histochemical and cell culture studies have shown that specific cell types or 

structures have metabolites that give rise to particular [1H]-MRS peaks. A change 

in the signal intensity of the peaks may reflect loss or damage of the specific cell 

type or a change in the NMR visibility of the metabolite (Davis et al, 2003). 

A typical MRS spectrum of adult brain is shown in figure 41 (spectra vary 

for newborns, children under 8 years and elderly). The spectrum is read from right 

to left with the first and tallest peak assigned to neuronal marker NA (N- 

acetylaspartate) resonating at 2 ppm. The second tallest resonance is Cr (creatine 

including phosphocreatine) resonating at ~3 ppm. Adjacent to the Cr peak is the 

smaller but important Ch (choline) peak. The ratio Ch/Cr of about 0.5 is 

characteristic of brain gray matter. Peaks corresponding to glucose and myoinositol 

(ml) are also seen in the spectrum of the normal adult brain (Davis et al, 2003). 

N-acetyl aspartate (2.01 ppm) 

The methyl resonance of NAA produces a large, sharp peak at 2.01 ppm. 

NAA is almost exclusively confined to neurons in the human brain, where it is 

found predominantly in axons and nerve processes. These cells represent only 2–3 

% of the glial population in man. The NAA peak therefore acts as a marker of 

healthy neurons. Reduction in the size of the NAA peak provides a useful indicator 

of neuronal disease or loss, including infarction after stroke. 

In children, the interpretation of the NAA signal is complicated by 

increases in the concentration of NAA during development when it is thought to 

have a role in supplying acetyl groups for myelin synthesis. In adults, the 

concentration is known to vary in different areas in the brain. For example, the 

concentration of NAA is higher in grey than white matter, which is explained by 

the higher neuronal density in grey matter. This can be overcome in the study of 

stroke patients by comparing spectra from an area of suspected abnormality with 

spectra from a homologous region of the contralateral normal hemisphere (Davis et 

al, 2003).

Creatine (3.94 and 3.03 ppm) 

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Both creatine and phosphocreatine have signals at 3.94 ppm (methylene 

singlet) and 3.03 ppm (methyl singlet) which makes it impossible to distinguish 

between the two compounds and therefore total creatine (Cr/PCr) signals are 

measured by [1H]-MRS. Other resonances seen at 3.00 ppm arise from the γ- 

amino butyric acid (GABA) and cytosolic macromolecules, which become 

incorporated into the Cr/PCr peak. Cr/PCr is found in both neurons and glial cells 

and acts as a phosphate buffer transport system and energy buffer within the cell. 

Little information can be gleaned about phosphocreatine metabolism because the 

signal comes from the sum of creatine and phosphocreatine. The complete absence 

of creatine signal probably reflects necrotic tissue (Davis et al, 2003). 

Choline (3.22 ppm) 

The trimethylamine resonance of choline-containing compounds is present 

at 3.22 ppm. In normal brain, the Cho peak is thought to consist predominantly of 

glycerolphosphocholine and phosphocholine. 

Both compounds are involved in membrane synthesis and degradation. 

Reduction in the choline peak has been proposed as a marker of membrane damage 


Lipid/macromolecule resonances 

Lipid peaks are detectable by short echo proton spectroscopy but are not 

seen at long echo times because they have short T2 decay constants and so the 

signal is lost at longer repetition times. 

Lipid/macromolecule peaks have been assigned at 0.9, 1.3 and 1.45 ppm in 

normal appearing brain .Increase in these resonances have been reported in stroke 

and demyelination. The 0.9 and 1.3 ppm resonances are assigned to the methylene 

and methyl groups of lipid, respectively (Davis et al, 2003).

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Fig.41 (Davis et al, 2003) Short echo time proton spectra (TE=30 ms, 

TR=2020 ms) obtained normal hemisphere. 

[H] MRS changes in cerebral ischemia 

MRS has been suggested to be more sensitive than MRI in detecting 

hypoxic damage. It has been proposed that MRS may be able to detect cerebral 

ischemia within seconds of its onset as compared to DWI that provides warning as 

early as 1 h after the onset (Davis et al, 2003). 

The most striking changes in patients with acute cerebral infarction on MRS 

is the appearance of lactate with reduction in NAA and total Cr/PCr within the 

infarct compared to the contralateral hemisphere. Large variations in the initial 

concentrations of Cho have been observed in the region of infarction (Davis et al, 

2003). 

The presence of a significant quantity of blood in the brain disrupts the 

homogeneity of the magnetic field due to the presence of the iron from the 

hemoglobin molecule, and spectroscopy cannot be carried out in patients with 

large intracerebral hemorrhages. However, it is possible to sufficiently shim the 

magnetic field away from areas of hemorrhagic transformation or subarachnoid 

hemorrhage and acquire spectra of acceptable line widths. Petechial hemorrhage 

may result in spectra with broader line widths due to field inhomogeneity, but the

spectra may still be of acceptable quality (Davis et al, 2003). 

Lactate (doublet at 1.33 ppm) 

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The detection of lactate on MRS, an end product of glycolysis, is a 

particularly useful measure of anaerobic metabolism. Lactate is not detected by 

MRS in normal brain. The concentration of lactate rises when the glycolytic rate 

exceeds the tissue’s capacity to catabolize it or remove it from the bloodstream. 

The rise in brain lactate that results from the mismatch between glycolysis and 

oxygen supply has been demonstrated by numerous [1H]-MRS experiments, 

making it an important hallmark for the detection of cerebral ischemia. The 

persistence of lactate for weeks or months after stroke onset is a common 

observation. Removal of lactate depends on the permeability of the blood–brain 

barrier (BBB) and diffusion of the metabolite through the damaged tissue. A fall in 

lactate concentration has been shown to occur during a period of hyperemia. 

Spectroscopic imaging studies have demonstrated that lactate is not confined to 

areas of infarction determined by T2-weighted imaging and in one study was even 

found in the contralateral hemisphere. In this study, the lactate levels in regions 

adjacent to infarcts as shown by T2 changes were not significantly different from 

those found in the infarcted brain. It seems likely that this is the result of diffusion 

of lactate out of the infarct, but the extent to which there is local production of 

lactate in peri-infarct tissue remains uncertain (Davis et al, 2003). 

Unfortunately, measurements within the core and penumbra of an infarct are 

not definitely different; moreover, the presence of Lac has a differential diagnosis 

including abscess. Lac evolution and/or resolution may be observed with or 

without an associated infarct (Gonzalez et al., 2006). 

NAA (2.01 ppm) 

Decreased NAA is most consistent with neuronal degradation, may occur 

very early in ischemia, is likely irreversible (as opposed to disease processes such 

as demyelination), and may continue for days to weeks even after the cessation of 

ischemia (Gonzalez et al., 2006). 

The continuing fall in NAA concentration over the course of the first week 

after stroke onset cannot be explained simply by an increase in edema because

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changes in the concentration of water within the infarct have been corrected for by 

using the contralateral water signal as the internal standard. It has been suggested 

that NAA is actively degraded by enzymes within the injured neurones in the first 

few days or hours following infarction. This remains a possibility but it seems 

unlikely that enzymes would remain active for up to 7–10 days within an ischemic 

neurone. The gradual decline in NAA concentration and the persistence of lactate 

within the region of infarction over a period of a number of days may suggest a 

period of ongoing ischemia and has implications in the timing of therapeutic 

intervention. Alternatively, it may reflect breakdown of NAA, removal by 

phagocytosis or diffusion, or alteration in the physicochemical surrounding of the 

metabolite associated with cell dissolution so that it is no longer MRS visible 


Correlation of NAA concentration to infarct size (volume) allows a better 

prediction of morbidity/ outcome than does either NAA concentration or infarct 

volume alone (Gonzalez et al., 2006). 

Cr/PCr (3.94 and 3.03 ppm) 

Initial reductions in Cr/PCr are identified following infarction and further 

reductions have been demonstrated up to 10 days following the time of onset. The 

pathological correlate is thought to be gliosis of the tissue. The reduction in NAA 

in the infarct region is more marked than the reduction in Cr/PCr and this is 

thought to reflect the increased sensitivity of neurons to ischemia, compared to 

glial tissue (Davis et al, 2003). 

Choline (3.22 ppm) 

The choline peak has been shown to be increased, decreased and stays the 

same following cerebral infarction. The changes in the choline peak are thought to 

reflect changes in the MR visibility of the choline containing compounds that make 

up the cell membrane. (Davis et al, 2003) have shown a fall and then a late rise, 

maximal 3 months after onset of stroke.This may represent loss of membrane 

function, followed by late gliosis (Davis et al, 2003). 

Glutamate and other amino acids 

It would be useful to be able to measure the concentration of excitotoxic

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amino acids, such as glutamate and glutamine, which are released in ischemia and 

may be responsible for neuronal injury in the penumbra. Glutamate and glutamine 

have strongly coupled spins and the chemical shift of 2.1–2.5 ppm at 1.5T overlaps 

with the NAA peak. Other amino acids, such as GABA, aspartate and alanine are 

also difficult to detect because of their low concentrations and/or overlap with 

more intense resonances from other compounds (Davis et al, 2003). 

Lipids/macromolecules 

Signals from lipids pose particular problems in [1H]-MRS by obscuring the 

resonances from the methyl group of lactate. It has been postulated that membrane 

lipids in the brain under normal conditions are not mobile enough to generate sharp 

spectral peaks in vivo. During ischemia, degradation of the membrane leads to the 

release of free fatty acids that produce well defined, but broad, resonances in the 

region of the lactate peak with resulting difficulties in the accurate quantification 

of lactate. The ‘metabolite nulling’ technique has been used to separate the lipid 

from the lactate signal (Davis et al, 2003). 

Advantages of MR spectroscopy: 

1. Potentially quantitative if external standards are used in addition to 

measurements on the patient (however, this may increase the time of the 

examination and further delay diagnosis and treatment of stroke – a 

liability). 

2. May be easily combined with conventional MR imaging, MR angiography, 

PWI and diffusion weighted imaging; these techniques are complementary. 

3. May be repeated immediately. 

4. No ionizing radiation exposure. 

5. Could theoretically improve differentiation in specific situations where the 

differential diagnosis includes tumor. 

6. Could potentially provide a surrogate marker for guiding stroke 

Liabilities 

thrombolysis (Gonzalez et al., 2006). 

1. The patient must have MR compatibility (that is, no pacemaker, cochlear 

implant, neurostimulator, etc.).

2. Motion artifact obviates interpretation. 

3. Low spatial resolution. 

4. Perfusion data are unavailable. 

5. Typically, the entire brain is not imaged. 

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6. Not all sites will have MR scanners readily available; furthermore, not all 

medical facilities will be able to offer this service round the clock (Gonzalez 

et al., 2006).

Patients and Methods 

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Patients & Methods 

This study was performed in the period from October 2007 till October 

2009 in Zagazig University Hospitals. Patients we referred from Emergency 

Unit, General Medicine and Neurology Departments. It included 50 stroke 

patients, 32 males and 18 females. Their ages ranged from 19 to 90 years. 

All patients were subjected to the following: 

1- Full history taking (from the patients or their relatives). 

*Accurate onset of neurological manifestation. 

*History of hypertension, diabetes mellitus, trauma or bleeding tendency. 

*Previous attacks of stroke. 

*Past history of allergy against contrast media like Gd-DTPA. 

2- Clinical assessment (by neurologist). 

3- Laboratory assessment (if needed) as: 

*Arterial blood gases to exclude electrolyte imbalance. 

*Blood sugar to exclude diabetic coma. 

*Prothrombin time. 

4- Computed tomography was performed on GE Hi-speed using axial cuts 

then the patients are divided into two groups according to the CT findings: 

a) Hemorrhagic stroke patients including 11 patients with intracerebral, 

intraventricular or subarachnoid hemorrhage. 

b) Ischemic stroke patients including 39 patients with or without evidence 

of infarction at CT. 

5- MR Imaging using Philips Achieva system (1.5 T). 

Ischemic stroke group 

These patients are chronologically classified into several groups: 

hyperacute (1 st 6 hours), Acute (6-24 hours), Early subacute (1-7 days), late 

subacute (1-2 weeks) and chronic (>2weeks) stages.

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Then all these patients (39 patients) were subjected to the following MRI 

sequences: 

1) Axial T1WI (TR148-597/TE2-15). 

2) Axial T2WI (TR4400-4800/TE110). 

3) Coronal T2WI (TR4400-4800/TE110). 

4) Axial Fluid attenuation inversion recovery (FLAIR) (TR6000/TE120- 

TI2000) for all ischemic stroke patients (39 patients). 

The previous sequences are done with slice section 5 mm with 1mm gap and 

Field of view (FOV) 230mm. 

5) Diffusion Weighted image (DWI) for all ischemic stroke patients (39 

patients): 

*The patients position is the same examining position of the brain MRI in the 

supine position with head coil. 

*Diffusion-weighted images were obtained using a multisection, single-shot 

echo-planar imaging sequence. 

*Section thickness was 5 mm with a gap of 1 mm. The number of sections was 

set to include the whole brain (average, 22). Matrix size was256 x128 ,(3100- 

3400/98-99/1 [TR/TE/excitation]), flip angle 90 degree and FOV 230mm . 

*Sensitization gradients are sequentially applied in the X, Y and Z planes.3 sets 

of images corresponding to sequential application of the sensitization gradient 

(b=1000) in the X, Y and Z planes, and a last set corresponding to the average 

images at b=1000. Typically, only 2 sets of images are used in clinical practice: 

the b=0 T2W images and the b=1000 average images. Scanning time was 1 

minute 15 seconds. 

*Apparent diffusion coefficient (ADC) maps were automatically calculated by 

MRI machine soft ware and included in the sequence.

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*Post Processing of DWI: region of interest (ROI) was selected in the area of 

infarction and comparative normal brain tissue. 

6) Perfusion weighted images (PWI) : for 17 (8 hyperacute, 8 acute and 1 

chronic) ischemic stroke patients. 

*The patients position is the same examining position of the brain MRI in the 

supine position with head coil. 

Perfusion-weighted images were obtained following administration of a bolus 

of gadopentetate dimeglumine 15 ml, the injection was performed by MRcompatible 

power injector at a speed of 4 mL/s followed by 20 ml of normal 

saline delivered via a large-bore cannula in the antecubital fossa. Imaging 

sequence at 26/19/1 (TR/TE/excitation) and flip angle of 7 degrees was used. 

(30) sections were obtained. Section thickness was3.5 mm with a 0 mm gap 

(matrix, 256 x 128; FOV 220 mm). Images were obtained at 60 time points per 

section with average scanning time 1 minute 24 seconds. 

Postprocessing of perfusion data: PWI images are transferred to workstation 

then color maps (TTP, MTT, T0) are generated automatically then the 

concentration time curve is obtained which represent the changes occurred. 

Firstly, ROI puts in the contralateral normal hemisphere as control normal 

region, and then multiple ROIs put in the different region of the lesion and 

surrounding it to see the extension of the lesion. 

Then obtaining of the quantitative measures of each ROI automatically or from 

the intensity time curve. 

7) Post contrast T1WI :for 11 patients of ischemic stroke patients.

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8) 2D & 3D time of flight MR angiography (TOF MRA) :TR:23-25, TE:7 , 

flip angle 20 degree, FOV 170-250 mm , slice thickness 1mm with gap 0.5 mm 

for 37 patients of ischemic stroke patients. 

9) MR venography (MRV): for 1 patient of hemorrhagic infarction. 

10) MR spectroscopy (MRS): for 34 patients of ischemic stroke patients. 

MRS was performed using the head coil. After global shiming performed with 

standered nonselective shiming sequence, the volume of interest (VOI) was 

localized in the infarcted area, taking care to avoid the inclusion of normal 

tissue or cerebrospinal fluid, and in the corresponding non affected 

contralateral region. The water proton signal was suppressed by a preceding 

chemical shift-selective radiofrequency pulse. The proton specta were acquired 

by means of a double spine-echo sequence. After Fourier tansformation and 

zero order phase correction, the areas under the peaks were obtained by 

numerical integration. Baseline correction was performed for the purpose of 

presentation. Resonance were assigned as follows: 

*Lactate (Lac) containing compounds at 1.3 ppm. 

*Choline (Cho) containing compounds at 3.2 ppm. 

*Creatine-phosphocreatine (Cr) containing compounds at 3.02 ppm. 

*N-acetyle aspartate(NAA) containing compounds at 2.02 ppm. 

Correlation between DWI and PWI lesions: 

*In aid of the DWI (b0 and b1000) for detection of the site of the 

infracted area, on PWI ;the ROIs put in the center of the lesions (infracted 

core, if present) and surrounding area (penumbra) and measure T0, TTP 

and MTT of each ROI then compared with the normal ROI measures.

- 87 - 


*DWI lesion volumes were determined by manually tracing the edge of 

the hyperintense signal on each slice of the trace DWI scans obtained at 

b=1000 s/mm 2 . The areas of hyperintensity were summed and multiplied 

with the slice thickness plus interslice gap to calculate the volume of the 

DWI abnormality. Then, volume of perfusion deficit measured from the 

TTP map in comparison with the contralateral side by the same method. 

DWI lesion volume is compared by PWI lesion volume. If the lesion 

volume in PWI is larger than DWI (DWI/PWI mismatch) subtraction of 

the DWI volume from PWI volume to obtain the penumbra volume. 

Hemorrhagic stroke group 

These patients are classified into several groups according to the site of 

hemorrhage : Intracerebral hemorrhage (7 patients), Subarachnoid hemorrhage 

(2 patients), Intraventricular hemorrhage (1 patient) and Intracerebral 

hemorrhage with intraventricular extension (1 patient).They are 

chronologically classified into hyperacute (1st 24 hours), acute stage for 2–3 

days, early subacute stage for 3–7 days, late subacute stage up to 2 weeks and 

chronic stage more than 2 weeks. Then these patients are subjected to the 

following MRI sequences: 

1) Axial T1WI . 

2) Axial T2WI . 

3) Axial Fluid attenuation inversion recovery (FLAIR). 

4) Axial Gradient images (T2*) (TR250/TE12). 

5) Diffusion Weighted image (DWI). 

6) 2D & 3D time of flight MR angiography (TOF MRA) for all hemorrhagic 

stroke patients and Phase contrast (Pc) MRA in 1 case of subarachnoid 

hemorrhage.

RESULTS 

RESULTS 

This study was performed on 50 patients .They were 32 males 

(64%) and 18 females (36%).Their ages ranged from 19to 90 years. 

Table (4):Age & Sex distribution among our patients. 

Age group 

(years) 

Age 

Patient 

NO. 

10- 1 2 

20- 1 2 

30- 1 2 

40- 8 16 

50- 11 22 

60- 19 38 

70- 7 14 

80- 2 4 

sex 

% sex Patient 

NO. 

Male 

Female 

Total 50 100 50 100 

The most common age group was 60-70 years (19 patients-38%) with 

mean age 59.6±14.1 years. 

-88- 

32 

18 

% 

64 

32

Table (5) Clinical presentation of our patients 

Clinical presentation No of 

patients 

RT sided hemiparesis 9 18 

RT sided hemiparesis with aphasia 4 8 

RT sided hemiplegia 10 20 

RT sided hemiplegia with aphasia 5 10 

LT sided hemiparesis 6 12 

LT sided hemiplegia 10 20 

Quadriparesis 4 8 

Headache with neck rigidity 2 4 

-89- 

RESULTS 

%

RESULTS 

Most of our cases were exposed to different risk factors 

including Hypertension, Ischemic heart disease, Diabetes mellitus, 

Hyperlipidaemia and smoking . Multiple risk factors can coexist in 

same patient. 

Table (6): Risk factors among our patients 

Risk factors No. Of patient % 

Hypertension 15 

Ischemic heart disease 

Ischemic heart disease with 

atrial fibrillation 

Diabetes mellitus 

Hyperlipidaemia 

Smoking 6 

7 

30 

14 

5 10 

Hypertension was the most common risk factor seen in 15 patients 

(30% of patients). 

9 

7 

-90- 

18 

14 

12

RESULTS 

Our patients were classified into 2 groups; Ischemic and Hemorrhagic 

stroke. 

Table (7): Classification of our patient: 

Type of stroke No. of patients % 

Ischemic stroke 

Hemorrhagic stroke 

Total 50 100 

39 

11 

Ischemic stroke patients were 39 patients (78%) however hemorrhagic 

stroke were 11 patients (22%). 

-91- 

78 

22

Ischemic stroke patients were classified into several groups 

according to the age of stroke. 

RESULTS 

Table (8):Chronological classification of ischemic stroke patients: 

Stage of infarction No. of patients % 

Hyperacute (1 st 6 hours). 10 25.6 

Acute (6-24 hours). 12 30.8 

Early subacute (1-7 days). 4 10.3 

Late subacute(1-2 weeks). 5 12.8 

Chronic (> 2 weeks). 8 20.5 

Total 39 100 

-92-

RESULTS 

Our ischemic stroke patients are subjected to different MRI 

sequences. 

Type of infarction 

Table (9): Different MRI sequences in ischemic stroke patients. 

No. of 

patient 

T1 T2 FLAIR MRA DWI PWI PCT1 MRV MRS 

Hyperacute 10 10 10 10 10 10 8 5 - 10 

Acute 12 12 12 12 12 12 8 4 - 10 

Early subacute 4 4 4 4 4 4 - - - 4 

Late subacute 5 5 5 5 3 5 - - 1 2 

Chronic 8 8 8 8 8 8 1 1 - 8 

Total 

% 

39 39 39 39 37 39 17 10 1 34 

100 100 100 100 95 100 46 26 2.6 87 

Perfusion weighted imaging (PWI) was done in only 17 

patients to show the presence or absence of the ischemic but 

still viable tissue (ischemic penumbra). 

Postcontrast T1(PCT1) was done in 10 patients only and 

showed arterial enhancement in 5 patients out of them. 

-93-

Stage of 

stroke Intensity Pt 

Hyperacute 

(10) 

RESULTS 

Table (10): Appearance of different ischemic stroke stages at 

different MRI sequences. 

*Not appear 

*Subtle intense 

Acute (12) *Not appear 

Early 

subacute(4) 

Late 

subacute(5) 


*hyperintense 

T2WI FLAIR DWI(b0) DWI(b1000) Exponential image ADC 

No 

3 

9 

1 

2 

7 

Intensity Pt 

*Not appear 


No 

6 

4 

Intensity Pt 

*Not appear 

*Subtle 

intense 

*Hyperintense 11 *Not appear 

*Subtle 

intense 

*hyperintense 

No 

1 

7 

3 

9 

2 

Intensity Pt 

*hyperintense 

ẽ brightness 

*hyperintense 

ẽ brightness 

No 

Intensity Pt 

No 

Intensity Pt 

No 

10 *hyperintense 10 hypointense 10 

12 *hyperintense 12 hypointense 12 

*hyperintense 4 *Hyperintense 4 *Hyperintense 4 *hyperintense 4 *hyperintense 4 hypointense 4 

*hyperintense 5 *Hyperintense 5 *Hyperintense 5 *hyperintense 5 *isointense 5 isointense 5 

Chronic(8) *hyperintense 8 *Hyperintense 8 *Hyperintense 8 *isointense 

-94- 

*hypointense 

6 

2 

*hypointense 8 hyperintense 8

stroke 

Table (11): Different ADC values in hyperacute ischemic 

Patient No ADC in infarction 

(10 -6 mm 2 /sec) 

ADC of contralateral 

normal area 

(10 -6 mm 2 /sec) 

1 354.62 814.95 

2 473.25 838.38 

3 480.54 959.51 

4 494 747.47 

5 370.72 731.85 

6 428.25 834.19 

7 405.49 722.03 

8 415.11 754.09 

9 320.82 790.60 

10 501.67 809.14 

RESULTS 

The mean ACD at the infarction site in hyperacute stage 

was 423.5410±63.7865 (mean±SD) while the mean ADC of the 

contralateral normal area was 800.2200±69.9746. There is a 

highly statistical significant difference between the ADC in 

infarction and contralateral normal site using T-test; t=15.383, 

p< 0.001. 

-95-

Table (12): Different ADC values in acute ischemic stroke 


(10 -6 mm 2 /sec) 


normal area 

(10 -6 mm 2 /sec) 

1 314.46 839.77 

2 363.02 823.91 

3 351.07 1155.22 

4 377.90 926.17 

5 367.72 1023.41 

6 236.71 668.48 

7 356.07 808.01 

8 319.14 739.22 

9 401.76 803.72 

10 235.25 762.23 

11 229.56 878.66 

12 342.11 911.87 

RESULTS 

The mean ACD at the infarction site in acute stage was 324.5642±59.5444 

while the mean ADC of the contralateral normal area was 869.9808±132.9708. 

There is a highly statistical significant difference between the ADC in infarction 

and contralateral normal site using T-test; t=15.555, p< 0.001. 

-96-

RESULTS 

Table (13): Different ADC values in early and late subacute ischemic 

stroke 

stage Patient 

No 

ADC in infarction 

(10 -6 mm 2 /sec) 


normal area 

(10 -6 mm 2 /sec) 

Early subacute 1 373.63 661.61 




Late subacute 1 872.54 816.92 





The mean ACD at the infarction site in early subacute stage was 

525.6575±144.9676 while the mean ADC of the contralateral normal area was 

740.5550±77.2328. There is a highly statistical significant difference between the 

ADC in infarction and contralateral normal site using T-test; t=6.340, p= 0.008. 

The mean ACD at the infarction site in late subacute stage was 

838.6140±58.2862 while the mean ADC of the contralateral normal area was 

827.7100±57.2120. There is no statistical significant difference between the ADC 

in infarction and contralateral normal site using T-test; t=0.862, p= 0.437. 

-97-

Table (14): Different ADC values in chronic ischemic stroke 


(10 -6 mm 2 /sec) 


normal area 

(10 -6 mm 2 /sec) 

1 1647.25 757.88 

2 1312.49 838.20 

3 3023.26 785.62 

4 1597.53 719.24 

5 1675.18 856.23 

6 1241.05 794.64 

7 1164.29 958.45 

8 2845.90 908.23 

The mean ACD at the infarction site in chronic stage was 

RESULTS 

1813.3688±719.4211 while the mean ADC of the contralateral normal 

area was 827.3112±79.2877. There is a highly statistical significant 

difference between the ADC in infarction and contralateral normal site 

using T-test; t=3.845, p= 0.006. 

-98-

RESULTS 

Table(15): Correlation between Mean ADC at the infarction 

and contralateral normal site in different ischemic stroke stages using 

Paired T test. 

Stage Patient 

No 

ADC in 

infarction 

[x - ±SD] 

(10 -6 mm 2 /sec) 

Hyperacute 10 423.5410± 

63.7865 

Acute 12 324.5642± 

Early 

subacute 

Late 

subacute 

4 

5 

59.5444 

525.6575± 

144.9676 

838.6140± 

58.2862 

Chronic 8 1813.3688± 

x - : is the mean 

719.4211 

SD: is the standered deviation. 

-99- 

ADC in 

contralateral 

normal site 

[x - ±SD] 

(10 -6 mm 2 /sec) 

800.2200± 

69.9746 

869.9808± 

132.9708 

740.5550± 

77.2328 

827.7100± 

57.2120 

827.3112± 

79.2877 

Paired T- 

test 

P value 

15.383

RESULTS 

Table(16):ADC and rADC correlation with different stages of infaction 

using ANOVA (f): 

ADC in infarction 

[x - ±SD] 

(10 -6 mm 2 /sec) 

rADC in infarction 

[x - ±SD] 

Hyperacute 423.5410± 63.7865 0.5308± 0.0899 

Acute 324.5642± 59.5444 0.3765± 0.06954 

Early subacute 525.6575± 144.9676 0.7002± 0.1231 

Late subacute 838.6140± 58.2862 1.0135± 0.03422 

normal site". 

Chronic 1813.3688± 719.4211 2.2094± 0.8806 

ANOVA (f) 28.193 28.280 

P value

RESULTS 

Fig 42(a)Scatterplot between the groups (stages) of ischemic stroke and 

ADC, (b)Scatterplot between the stages of ischemic stroke and rADC(ADC ratio) 

where 1 is hyperacute , 2 is acute stage ,3 is early subacute, 4 is late subacute and 

5 is chronic stages.The rADC starts to decrease (

RESULTS 

Most of hyperacute and acute ischemic stroke patients (17 patients) 

are subjected to PWI. 

17 patients. 

Table (17): Relation between lesion volumes in DWI & PWI in 

Pattern No of patient 

PWI > DWI (diffusion 

perfusion mismatch with 

penumbrae) 

PWI = DWI (matched) 

Hyperacute (5 patients) 

Acute (3 patients) 

Hyperacute (2 patients) 

Acute (3 patients) 

Chronic (1 patient) 

8 

6 

Arterial 

distribution 

ICA(1 patient) 

MCA(6patients) 

PCA(1 patient) 

ICA(1 patient) 

MCA(3patients) 

PCA(1 patient) 

ACA(1 patient) 

PWI < DWI Acute 2 MCA(2patients) 

DWI but no PWI Hyperacute 1 Pontine branch 0f 

basilar artery (1 

Total 17 

-102- 

patient)

RESULTS 

Table (18): Mean transit time (MTT) values in patients with 

diffusion perfusion mismatch. 

Patient 

No. 

Stage MTT at 

penumbra(sec) 

MTT at normal 

contralateral 

area(sec) 

1 Hyperacute 19 11.5 

2 Hyperacute 22 16 


4 Hyperacute 16.5 10.2 


6 Acute 18 11 

7 Acute 19.6 11.4 

8 Acute 15.2 9.3 

The mean MTT at penumbra in diffusion perfusion 

mismatched cases was 17.6250±2.7675 while the mean MTT of 

the contralateral normal area was 10.6000±2.8087. There is a 

highly statistical significant difference between the MTT at 

penumbra and contralateral normal site using T-test; t=21.329, 

p< 0.001. 

-103-

Table (19): Time to peak (TTP) values in patients with 

diffusion perfusion mismatch. 

Patient 

No. 

Stage TTP at 

penumbra(sec) 

RESULTS 

TTP at normal 

contralateral 

area(sec) 

1 Hy.peracute 49 44 


3 Hyperacute 32.5 26 



6 Acute 42.5 30 

7 Acute 41.4 32.6 

8 Acute 36.8 30.5 

The mean TTP at penumbra in diffusion perfusion 

mismatched cases was 44.7875±12.1561 while the mean TTP of 

the contralateral normal area was 35.9375±11.2246. There is a 

highly statistical significant difference between the mean TTP 

at penumbra and contralateral normal site using T-test; t=9.154, 

p< 0.001. 

-104-

RESULTS 

Table(20): Correlation between Mean MTT and TTP at the 

infarction and contralateral normal site using Paired T test. 

Stage Patient 

No 

Penumbra 

[x - ±SD] 

MTT (sec) 8 17.6250± 

2.7675 

TTP (sec) 8 44.7875± 

12.1561 

-105- 

contralateral 

normal site 

[x - ±SD] 

10.6000± 

2.8087 

35.9375± 

11.2246 

Paired T- 

test 

P value 

21.329

RESULTS 

Table (21): MRA findings in different types of ischemic stroke 

patients (37 patients). 

Type of stroke 

Hyperacute 

Positive 

(occlusion) 

8 

MRA 

Negative Total 

2 

10 

Distribution(+ve) 

Both ICAs (1 patient) 

Rt ICA (1 patient) 

Rt MCA(1 patient) 

Lt MCA(3 patients) 

Rt PCA(1 patients) 

Both PCA(1 patient) 

Acute 4 8 12 Rt MCA(1 patient) 

Lt MCA(3 patients) 

Early subacute 2 2 4 Rt MCA(2 patients) 

Late subacute 1 2 3 Lt MCA 

Chronic - 8 8 - 

Total 15 22 37 - 

MRA was positive (occlusion) in 15 out of 37 patients mainly 

in the hyperacute (8 out of 10 patients) and acute (4 out of 8 patients) 

stages. 

-106-

RESULTS 

Table (22): Post contrast T1WI findings in different types of 

ischemic stroke patients (11 patients). 

Type of stroke 

Hyperacute 

Acute 

Chronic 

Positive 

+ ++ 

1 

2 

- 

2 

- 

- 

PCT1 


Total 3 2 5 10 

Postcontrast T1(PCT1) was done in 10 patients only and 

showed arterial enhancement in 5 patients out of them (2 patients 

showed marked enhancement and 3 patients showed mild 

enhancement) 

-107- 

2 

2 

1 

5 

4 

1

RESULTS 

Table (23): MR spectroscopic findings in ischemic stroke patients(34 

patients). 

Stage No Lactate iNAA/cNAA iCr/cCr iCho/cCho 

Hyperacute 1 + 0.09 0.46 0.92 

Hyperacute 2 + 0.21 0.08 0.76 

Hyperacute 3 + 0.02 0.62 0.45 

Hyperacute 4 + 0.81 1.05 0.88 

Hyperacute 5 + 0.43 0.31 0.94 

Hyperacute 6 + 0.19 0.37 0.77 

Hyperacute 7 + 0.01 0.07 0.21 

Hyperacute 8 + 0.68 1.03 0.73 

Hyperacute 9 + 0.32 0.23 0.85 

Hyperacute 10 + 0.56 0.92 0.91 

Acute 11 + 0.72 0.77 0.42 

Acute 12 + 0.61 1.00 1.13 

Acute 13 + 0.01 0.48 0.44 

Acute 14 + 0.08 0.63 0.07 

Acute 15 + 0.37 0.09 0.36 

Acute 16 + 0.45 0.95 1.06 

Acute 17 + 0.21 0.08 0.74 

-108-

Acute 18 + 0.17 1.12 0.96 

Acute 19 + 0.05 0.01 0.81 

Acute 20 + 0.57 0.69 1.21 

Early subacute 21 + 0.46 0.65 0.86 


Early subacute 23 - 0.51 0.43 0.46 


Late subacute 25 - 0.82 0.02 0.91 

Late subacute 26 + 0.91 0.89 0.84 

Chronic 27 + 0.24 0.81 0.27 

Chronic 28 + 0.52 0.64 0.48 

Chronic 29 - 0.34 0.43 1.72 

Chronic 30 + 0.83 1.13 0.92 

Chronic 31 - 0.64 0.77 1.09 

Chronic 32 - 0.76 0.61 1.56 

Chronic 33 - 0.21 1.27 1.66 

Chronic 34 + 0.92 0.93 0.88 

RESULTS 

iNAA indicates N-acetylaspartate from infarcted area; cNAA:N-acetylaspartate 

from contralateral area, iCr: creatine-phosphocreatine from infarcted area, cCr: 

creatine-phosphocreatine from contralateral area, iCho: choline-containing 

compounds from infarcted area, cCho: choline-containing compounds from 

contralateral area, Lac: lactate; +: present; -: absent. 

-109-

RESULTS 

Table(24):MR spectroscopic lactate findings correlation with different 

stages of infaction using Chi-Sguare test (X 2 ): 

Stage Hyperacute Acute Early 

Patient 

No. 

Lactate 

+ve 

Lactate 

-ve 

subacute 

Late 

subacute 

Chronic 

10 10 4 2 8 

10 

100% 

10 

100% 

3 

75% 

0 0 1 

25% 

X 2 11.637 

P value 0.020 

1 

50% 

1 

50% 

4 

50% 

4 

50% 

There is a statistical significant difference in lactate level 

among different stroke stages (p

RESULTS 

Table(25):MR spectroscopic findings correlation with different stages of 

infaction using ANOVA (f): 

Patient 

No. 

Mean iNAA/cNAA 

[x - ±SD] 

Mean iCr/cCr 

[x - ±SD] 

Hyperacute 10 0.3320± 0.2801 0.5140± 

0.3743 

Acute 10 0.3270± 0.2593 0.5830± 

Early 

subacute 

Late 

subacute 

0.4071 

4 0.3400± 0.1971 0.3700± 

0.2371 

2 0.8650± 0.0636 0.4550± 

0.6152 

Chronic 8 0.5575± 0.2735 0. 8238± 

0.2782 

Mean iCho/cCho 

[x - ±SD] 

0.7420± 0.2356 

0.7200± 0.3816 

0. 7875± 0.3261 

0.8750± 0.0495 

1.0725± 0.5422 

ANOVA (f) 2.730 1.368 1.176 

P value 0.048 0.269 0.342 

There is a statistical significant difference in NAA level among 

different stroke stages(p

Table (26): LSD (least significant difference) for Mean iNAA/cNAA 

comparison between different ischemic stroke stages. 

Hyperacute Acute Early 

subacute 

RESULTS 

Late 

subacute 

Acute >0.05 - - - 

Early subacute >0.05 >0.05 - - 

Late subacute 0.05 >0.05 

LSD revealed that late subacute stage is statistically significant higher 

than hyperacute, acute and early subacute stages. 

-112-

patients). 

RESULTS 

Table (27):Classification of hemorrhagic stroke patients (11 

Type of hemorrhage No % 

ICH 

SAH 

IVH 

Total 12 

8 

2 

2 

72.7 

The number of hemorrhagic stroke patients was 11 patients 

however the number of lesions was 12 as there is one patient had ICH 

with intraventricular extension. 

-113- 

18 

18

Stage of 

hematoma 

Hyperacute 

(1 st 24 

hours) 

Acute (1 st 

2-3 days) 

Early 

subacute 

(3-7days) 

Late 

subacute 

(1-2 

weeks) 

Chronic 

(>2weeks) 

Table (28): Signal intensity of cases of intracerebral hematoma in 

different MRI sequences. 

No Degree 

of 

edema 

2 + iso ↑ 

2 + Iso 

T1 T2 GRE (T2 * ) 

with↓rim 

with↓rim 

heterogenous 

↑ 

FLAIR 

↑ 

with↓rim 

RESULTS 

DWI 

b 0 b 

↑ with↓ 

rim 

1000 

ADC 

map 

↑ ↓ 

↓ ↓ ↓ ↓ ↓ ↓ 

1 + ↑ ↓ ↓ ↓ ↓ ↓ ↓ 

2 - ↑ ↑ ↑ ↑ ↑ ↑ ↑ 

1 - ↓with↑ 

center 

↓with↑ 

center 

Iso=intermediate signal intensity. 

↑=high signal intensity. 

↓=low signal intensity. 

-114- 

↓with↑ 

center 

↓with↑ 

center 

↓with↑ 

center 

↓ ↑

RESULTS 

Table (29): Detection of subarachnoid hemorrhage by different MRI 

sequences. 

Patient 

No. 

1 st 

patient 

2 nd 

patient 

onset T1 T2 GRE 

(T2 * ) 

FLAIR 

DWI 

b 0 b 

1000 

ADC 

map 

5 days ++ + + ++ + + + 

6 days - - - + - - - 

-115-

RESULTS 

Table (30):Signal intensity of cases of intraventricular in different 

MRI sequences. 

Patient 

No. 

1 st 

patient 

2 nd 

patient 

onset T1 T2 GRE 

(T2 * ) 

FLAIR 

b 

0 

DWI 

b 

1000 

ADC 

hyperacute iso ↑ ↑ ↑ ↑ ↑ ↓ 

map 

Acute iso ↓ ↓ ↓ ↓ ↓ ↓ 

Iso=intermediate signal intensity. 

↑=high signal intensity. 

↓=low signal intensity. 

-116-

-117- 

RESULTS 

Table (31): MRA findings in different types of hemorrhagic stroke. 

Site of hemorrhage 

Non 

filling 

Positive 

MRA 

spasm aneurysm Total 


Intracerebral(8) 1 2 - 3 5 8 

Subarachnoid(2) - 1 1 2 - 2 

Intraventricular(1) - - - - 1 1 

Total 1 3 1 5 6 11

Stage of 

stroke 

Hyper- 

acute(10) 

Acute (12) 

Early subacute 

(4) 

Late subacute 

(5) 

Chronic 

(8) 

Table (10): Appearance of different ischemic stroke stages at different MRI sequences. 

T2WI 

Intensity 

Not appear 

Subtle intense 

Not appear 


hyperintense 

hyperintense 

hyperintense 

hyperintense 

Pt. 

No. 

9 

1 

2 

7 

3 

4 

5 

8 

Intensity 

Not appear 

FLAIR 


Hyperintense 

Hyperintense 

Hyperintense 

Hyperintense 

Pt. 

No. 

4 

6 

11 

4 

5 

8 

Intensity 

Not appear 

DWI(b0) 


Not appear 


Hyperintense 

Hyperintense 

Hyperintense 

Hyperintense 

-94- 

Pt. 

No 

9 

1 

2 

7 

3 

4 

5 

8 

DWI(b1000) 

Intensity 

hyperintense ẽ 

brightness 

hyperintense ẽ 

brightness 

hyperintense 

hyperintense 

isointense 

hypointense 

Pt. 

No. 

10 

12 

4 

5 

2 

6 

Exponential 

image 

Intensity 

hyperintense 

hyperintense 

hyperintense 

isointense 

hypointense 

Pt. 

No. 

10 

12 

4 

5 

8 

RESULTS 

ADC 

Intensity 

hypointense 

hypointense 

hypointense 

Isointense 

hyperintense 

Pt. 

No 

10 

12 

4 

5 

8

-94- 

RESULTS

Illustrative cases 

- 118 - 


Case 1 (Fig.43): Hyperacute ischemic stroke with D/P mismatch and 

penumbra. 

Female patient, 90 years old presented with quadriplegia. 

MRI was done 6 hours after clinical presentation. 

(a) T1WI is normal. T2WI (b) and FLAIR (c) show subtle increase signal 

intensity involving most of the left cerebral hemisphere. 

(d) DWI (b1000) shows abnormal signal intensity lesion involving most 

of the left cerebral hemisphere and a small area in the right and right 

basal ganglia regions displaying high signal intensity with brightness 

(restricted diffusion). 

(e) Exponential image shows hyperintense signal in the same area. 

(f) ADC map shows low signal intensity of the same area. 

(g-k) perfusion maps show a larger lesion in the left cerebral hemisphere 

with central dead area and surrounding zone of hypoperfusion (delayed 

TTP and increased MTT). 

(l) Time signal intensity curve shows: ROIs reveal normal one (area 1) 

showing T0=37 sec, TTP=44 sec and MTT=11.5 sec.The central area 

(area 2) shows flat curve with no cerebral blood flow. The peripheral area 

(area 3) shows wide curve with delayed TTP=49 sec (delay 5 sec from 

normal curve), increase MTT=19 sec (increase 7.5 sec from normal 

curve). 

(m) axial and (n) coronal 3D TOF MRA show non filling of both ICAs. 

Right posterior cerebral artery (PCA) is slightly compansatory 

hypertrophied to supply the right cerebral hemisphere through anastmosis 

with the right posterior communicating artery. The left posterior cerebral 

artery is not good visualized. 

(o) MR spectroscopy (MRS) of the infarction site shows presence of 

lactate, decreased level of NAA, creatine and choline.

- 119 - 

Illustrative cases

- 120 - 

Illustrative cases

- 121 - 

Illustrative cases

- 122 - 


Case 2 (Fig.44): Hyperacute ischemic stroke with D/P mismatch and 

penumbra. 

Male patient, 72 years old presented with right sided hemiplegia. 

MRI was done 5 hours after clinical presentation. 

(a) Axial CT is completely normal. 

Axial T1 (b) and T2WI (c) are completely normal. 

(d) Axial FLAIR shows subtle intensity at the left high parietal region. 

DWI-b0 (e) is normal however DWI-b1000 (f) shows hyperintense lesion 

with brightness at the left high parietal region. The infarction shows 

hyperintensity at exponential image (g) and low signal intensity at ADC 

map (h). 

Perfusion Weighted Images (i-m) show larger lesion in the left parital 

region with central dead area and peripheral are of hypoperfusion. 

(n) Time signal intensity curve shows 3ROIs. ROI 1 shows normal curve 

with TTP 60 sec and MTT 16 sec. ROI2 (central dead area) shows 

flattened curve with no cerebral blood flow. ROI 3 (peripheral 

hypoperfused area) shows wide curve with TTP 72 sec and MTT 22 sec 

[delayed TTP 12 sec and increased MTT 6 sec in comparison with the 

normal curve]. 

Axial (o) and coronal (p) 3D TOF MRA show obstruction of some of the 

cortical branches of the left Middle Cerebral Artery (MCA) and non 

filling of the right Anterior Cerebral Artery (ACA). 

(q) MRS of the infarction show presence of small amount of lactate, 

reduction of the level of NAA, creatine and choline.

- 123 - 

Illustrative cases

- 124 - 

Illustrative cases

- 125 - 

Illustrative cases

Case 3 (Fig.45): Hyperacute ischemic stroke with D/P matching. 

Male patient, 59 years old presented with left sided hemiplegia. 

- 126 - 


Radiological examination was done 5 hours after clinical presentation. 


Axial T1 (b) and T2WI (c) and FLAIR (d) are completely normal. 

(e) DW images-b0 are completely normal however DWI-b1000 (f) show 

multiple infarcts displaying high signal intensity with brightness 

(restricted diffusion) at the right temporal, right midbrain and both 

thalamic regions. 

At exponential images (g) the lesions are hyperintense however they are 

of low signal intensity at ADC maps (h). 

PW images (I1-5) show the infarcted region as seen on DWI(D/P 

matching). 

Time signal intensity curve (I6) shows the infarcted area (area 2) 

represented by flat curve with no CBF and the normal contralateral area 

(area 2) represented by normal curve with T0=26sec, TTP=32 sec and 

MTT=9sec. 

Axial and coronal 3D TOF MRA (j) show occlusion of right Posterior 

cerebral artery (PCA) with non filling of right posterior communicating 

artery. 

MRS at the infarction site (k) shows presence of lactate and reduction of 

NAA, creatine and choline levels.

- 127 - 

Illustrative cases

- 128 - 

Illustrative cases

- 129 - 

Illustrative cases

Case 4 (Fig. 46): Hyperacute ischemic stroke with D/P matching. 

Male patient, 74 years old presented with left sided wakness. 



Axial T1W images (b&c) are normal. 

- 130 - 


T2WI (d) and FLAIR (e) show subtle area of increased signal intensity at the 

right basal ganglia (right lentiform). 

DW image-b0 (f) is normal however DWI-b1000 (g-h) show high signal 

intensity area with brightness (restricted diffusion) at the right basal ganglia 

and periventricular regions mainly at the right side. 

At exponential images (i-j) the infarction is hyperintense however they are of 

low signal intensity at ADC maps (k-l). 

Post contrast T1W images (m-n) show right cortical vascular enhancement at 

the disterbution of right MCA. 

PW images (o-s) show the infarction size as seen on DWI (D/Pmatching). 

Time signal intensity curve (t) shows ROIs revealing :ROI 1 on the infarcted 

area is represented by flat curve with no cerebral blood flow ,ROI 3 on the 

contralateral normal area revealing normal curve with T0=24 sec, TTP=30.2 

sec and MTT=11.7 sec and ROI 2 on the normal area surrounding the 

infarction revealing normal curve with T0=22.9 sec, TTP=30.4 sec and 

MTT=11.4 sec. Axial (u) and coronal (v) 3D TOF MRA show obstruction of 

the right ICA with filling of the right MCA and ACA from contralateral ICA 

through the circle of Wills associated with attenuation of right ACA and MCA 

and their branches. 

MRS (v) of the infarcted area showspresence of lactate, reduction of NAA and 

creatine levels with slight increase in choline level.

- 131 - 

Illustrative cases

- 132 - 

Illustrative cases

- 133 - 

Illustrative cases

- 134 - 

Illustrative cases

- 135 - 


Case 5 (Fig. 47): Hyperacute ischemic stroke DWI lesion without PWI 

abnormality. 

Female patient, 80 years old presented with coma. 



Axial T1W images (b) , T2WI (c) and FLAIR (d) are normal. 

DW image-b0 (e) is normal however DWI-b1000 (f) shows high signal 

intensity area with brightness (restricted diffusion) at the left side of pons. 

At exponential images (g) the infarction is hyperintense however it is of 

low signal intensity at ADC maps (h). 

On PW images (i-m) there is no apparent perfusion abnormality. 

Time signal intensity curve (n) : ROI 1at the infarction site on DWI 

shows normal curve with TTP=30 sec and MTT=11 sec and ROI 2 on 

normal site on DWI shows normal curve with TTP=31 sec and MTT=10 

sec. 

Coronal 3D TOF MRA (o) shows no apparent abnormality . 

MRS (p) of the infarcted area showspresence of lactate, reduction of 

NAA and creatine levels with normal choline level.

- 136 - 

Illustrative cases

- 137 - 

Illustrative cases

- 138 - 

Illustrative cases

Case 6 (Fig.48): Hyperacute ischemic stroke . 

- 139 - 


Female patient, 80 years old presented with right sided hemiplegia. 



Axial T1W image (b) is completely normal. 

T2WI (c) and FLAIR (d) and DW image-b0 (e) show mild 

hyperintensity of the left basal ganglia (left lentiform). 

DWI-b1000 (f) show high signal intensity area with brightness (restricted 

diffusion) at the left basal ganglia. 

At exponential images (g) the infarction is hyperintense however they are 

of low signal intensity at ADC maps (h). 

Post contrast coronal T1W images (i-j) show left cortical vascular 

enhancement at the disterbution of left MCA. 

Axial non enhanced CT cuts at the level of the left MCA (k-l) show 

hyperattenuation along the proximal segment of the left MCA(hyperdense 

MCA sign) denoting dense thrombus. 

Axial 2D TOF MRA (m) shows absence of flow of the left MCA. 

Axial (n) and coronal (o) 3D TOF MRA show obstruction of the 

proximal segment of the left MCA (M1). 

MRS (p) of the infarcted area shows presence of lactate, reduction of 


- 140 - 

Illustrative cases

- 141 - 

Illustrative cases

- 142 - 

Illustrative cases

Case 7 (Fig.49): Hyperacute ischemic stroke . 

Male patient, 69 years old presented with coma. 

- 143 - 



(a) Axial non enhanced CT cuts are completely normal. 

Axial T1W images (b) are normal. 

T2WI (c) and FLAIR (d) and DW images-b0 (e) show small faintly 

intense lesions at both thalami. 

DW images-b1000 (f) show multiple hyperintense lesions with brightness 

(restricted diffusion) at right occipital, midbrain and both thalamic 

regions. 

At exponential images (g) the infarctions are hyperintense however they 

are of low signal intensity at ADC maps (h). 

Axial (i) and coronal (j) 3D TOF MRA show non filling of the distal 

basilar and right posterior cerebral artery (PCA). The left PCA is not well 

visualized (filling from the left posterior communicating artery). The 

proximal segment of the left anterior cerebral (A1) is not visualized. 

MRS (k) of the infarcted site shows presence of lactate, slight reduction 

of NAA and creatine levels with normal choline level.

- 144 - 

Illustrative cases

- 145 - 

Illustrative cases

- 146 - 

Illustrative cases

Case 8 (Fig.50): Acute ischemic stroke with D/P matching. 

Male patient, 65 years old presented with rigt sided wakness. 

- 147 - 



(a) Axial CT shows faint ill defined hypodense area at the left basal 

ganglia (left caudate nucleus). 

Axial T1W image (b) shows faint hypointense area at the left caudate 

nucleus. 

Axial T2WI (c) ,FLAIR (d) and DW images-b0 (e) show subtle area of 

increased signal intensity at the left basal ganglia . 

DWI-b1000 (f) shows hyperintense infarction with brightness (restricted 

diffusion) at the left basal ganglia(left caudate nucleus and lentiform) . 

At exponential images (g) the infarction displays high signal intensity 

however on ADC map (h) it displays low signal intensity. 

PW images (i-m) show the infarction size as seen on DWI 

(D/Pmatching). 

Time signal intensity curve (n) : ROI 2 on the infarcted area is 

represented by flat curve with no cerebral blood flow ,ROI 1 on the 

contralateral normal area revealing normal curve with T0=24.9 sec, 

TTP=31.8 sec and MTT=10 sec and ROI 3 on the normal area 

surrounding the infarction revealing normal curve with T0=26.6 sec, 

TTP=33.1 sec and MTT=9.8 sec. 

Post contrast T1WI (o) is normal. 

Coronal 3D TOF MRA (p) shows no abnormality. 

MRS (q) of the infarcted area showspresence of lactate, reduction of 

NAA and creatine and choline levels.

- 148 - 

Illustrative cases

- 149 - 

Illustrative cases

- 150 - 

Illustrative cases

Case 9 (Fig. 51 ): Acute ischemic stroke. 

Male patient, 47 years old presented with right sided wakness. 

- 151 - 



Axial T1W image (a) shows small faint hypointense area at the left basal 

ganglia. 

Axial T2WI (b) ,FLAIR (c) and DW images-b0 (d) show mildly intense 

small lesion at the left basal ganglia. 

The lesion is markedly hyperintense with brightness on DWI-b1000 (e) 

and hyperintense on exponential images (f). On ADC map (g) it displays 

low signal intensity. 

PW images (k-h) show the infarction size as seen on DWI 

(D/Pmatching). 

Time signal intensity curve (l) : ROI 1 on the infarcted area is represented 

by flat curve with no cerebral blood flow however ROI 2 on the 


TTP=31.9 sec and MTT=9.2 sec . 

Post contrast T1WI (m) is normal. 

Axial (n) and coronal (o) 3D TOF MRA show no abnormality. 



- 152 - 

Illustrative cases

- 153 - 

Illustrative cases

- 154 - 

Illustrative cases

Case 10 (Fig. 52): Acute ischemic stroke . 

Female patient, 45 years old presented with left sided wakness. 

- 155 - 



(a) Axial CT shows subtle small hypodense area at the right lateral aspect 

of pons. 

Axial T1W image (b) is normal. 

Axial T2WI (c) ,FLAIR (d) and DW images-b0 (e) show subtle intensity 

at the right lateral aspect of pons . 

DWI-b1000 (f) shows small bright hyperintense infarction (restricted 

diffusion) at the right lateral aspect of pons). 

At exponential images (g) the infarction displays high signal intensity 

however on ADC map (h) it displays low signal intensity. 

Coronal 3D TOF MRA (i) shows no abnormality. 

MRS (j) of the infarcted area showspresence of lactate, reduction of 

NAA,normal creatine and increased choline levels.

- 156 - 

Illustrative cases

- 157 - 

Illustrative cases

Case 11 (Fig.53): Acute ischemic stroke . 

Female patient, 60 years old presented with dysarthria. 

- 158 - 



(a-b) Axial CT cuts are normal. 

Axial T1W image (c) is normal. 

Axial T2WI (d) ,FLAIR (e) and DW images-b0 (f) show mild 

hyperintensity at the right high parietal region . 

DWI-b1000 (g) shows bright hyperintense infarction (restricted diffusion) 

at the right high parietal region). 

At exponential images (h) the infarction displays high signal intensity 

however on ADC map (i) it displays low signal intensity. 

Axial 3D TOF MRA (j) shows no apparent abnormality. 

MRS (k) of the infarcted area shows presence of lactate, reduction of 


- 159 - 

Illustrative cases

- 160 - 

Illustrative cases

Case 12 (Fig.54): Subacute ischemic stroke . 

Male patient, 40 years old presented with ataxia. 

- 161 - 


Radiological examination was done 8 days after clinical presentation. 

Axial T1W image (a) shows small hypointense area at the right cerebellar 

hemisphere adjacent to the fourth ventricle. 

The infarction shows high signal intensity at axial T2WI (b) ,FLAIR (c) 

and DW images-b1000 (d). 

It displays nearly intermediate signal intensity at exponential images (e) 

and ADC map (f).

- 162 - 

Illustrative cases

Case 13 (Fig.55): Chronic ischemic stroke . 

Male patient, 27 years old presented with left sided hemiplegia. 

- 163 - 


Radiological examination was done 1 month after clinical presentation. 

(a) Axial CT shows an ill defined hypodense area of infarction at the 

right basal ganglia. 

The infarction is of low signal intensity at axial T1WI (b) and high signal 

intensity at axial T2WI (c) ,FLAIR (d) and DW images-b0 (e) however it 

is isointense on DWI-b1000 (f) , low signal intensity at exponential image 

(g) and high signal intensity on ADC map (h). 

Coronal 3D TOF MRA (i) shows no apparent abnormality. 

MRS (k) of the infarcted area shows presence of lactate, reduction of 

NAA and creatine levels with increase in choline level.

- 164 - 

Illustrative cases

- 165 - 

Illustrative cases

Case 14 (Fig.56): Chronic ischemic stroke . 

Male patient, 65 years old presented with left sided weakness. 

- 166 - 


Radiological examination was done 6 monthes after clinical presentation. 

(a) Axial CT shows a well defined hypodense area of infarction at the 

right high patietal region. 

The infarction is of low signal intensity at axial T1WI (b) and high signal 

intensity at axial T2WI (c) ,FLAIR (d) and DW images-b0 (e). At DWIb1000 

(f) the infarction displays low to intermediate signal intensity 

however at exponential image (g) it displays low signal intensity and high 

signal intensity at ADC map (h). 

PW images (i-m) show the non perfused infarcted area. 

Time signal intensity curve (n) : ROI 2 on the infarcted area is 

represented by flat curve with no cerebral blood flow ,ROI 1 on the 


TTP=33.9 sec and MTT=11.8 sec and ROI 3 on the normal area 

surrounding the infarction revealing normal curve with T0=26.1 sec, 

TTP=34.1 sec and MTT=12.3 sec. 

Post contrast axial T1WI (o) shows no vascular or parenchymal 

enhancement. 

Coronal 3D TOF MRA (o) shows no abnormality. 


NAA and creatine levels with increase in choline level.

- 167 - 

Illustrative cases

- 168 - 

Illustrative cases

- 169 - 

Illustrative cases

Case 15 (Fig.57): Hyperacute intracerebral hemorrhagic stroke . 


- 170 - 



(a) Axial non enhanced CT shows fresh blood density at both basal 

ganglia regions associated with intraventricular extension. 

MRI through the level of the left basal ganglia hematoma shows 

abnormal signal intensity lesion at the left basal ganglia surrounded by 

mild perifocal oedema, causing effacement of the left lateral ventricle and 

associated with intraventricular extension displaying the same signl 

intensity. 

The lesion displays intermediate to low signal intensity at axial T1WI (b), 

high signal intensity surrounded by low signal intensity rim at T2WI (cd) 

and FLAIR (f) and heterogenous signal intensity at GRE image (e). 

The lesion displays high signal intensity at DWI-b1000 (g) and 

exponential image (h) and low signal intensity on ADC map (i). 

Axial (j) and coronal (k) 3D TOF MRA show non visualization of the 

left MCA with non good visualization of both lenticulostriate arteries.

- 171 - 

Illustrative cases

- 172 - 

Illustrative cases

Case 16 (Fig.58): Acute intracerebral hemorrhagic stroke . 


MRI examination was done 3 days after clinical presentation. 

- 173 - 


It shows abnormal signal intensity lesion (hematoma) at the left parieto- 

occipital region, surrounded by mild perifocal oedema,and causing mass 

effect in the form of effacement of the left lateral ventricle . 

It displays low signal intensity with high signal intensity peripheral zone 

(peripheral intracellular methemoglobin of early subacute hemorrhage) at 

axial T1WI (a) and low signal intensity at T2WI (b) , FLAIR (c) and 

DWI-b0 (d). It also displays low signal intensity at DWI-b1000 (e) due to 

magnetic susceptability effect and low signal intensity on ADC map (f). 

Axial (g) and coronal (h) 3D TOF MRA show the hematoma as well as 

attenuation os the distal cortical segment of left MCA.

- 174 - 

Illustrative cases

- 175 - 

Illustrative cases

- 176 - 


Case 17 (Fig.59): Late subacute intracerebral hemorrhagic stroke . 

Male patient, 41 years old presented with right sided weakness. 

MRI examination was done 13 days after clinical presentation. 

It shows abnormal signal intensity lesion (hematoma) at the left basal 

ganglia, surrounded by mild perifocal oedema. 

It displays high signal intensity at axial T1 (a) , T2WI (b) , FLAIR (c) , 

DWI-b0 (d) , DWI-b1000 (e) and ADC map (f).

- 177 - 

Illustrative cases

- 178 - 


Case 18 (Fig.60):Subarachnoid hemorrhage (SAH) with rupture 

inracranial aneurysm. 

Female patient, 59 years old presented with sever headche, vomiting and 

confusion. 

Axial CT examination (a-b) done 4 hours after presentation shows fresh 

blood density at the subarachnoid space of the basal cisterns associated 

with mild hydrocephalic changes. 

MRI examination done 6 days after clinical presentation the 

subarachnoid hemorrhage can not be seen at all MR sequence except 

FLAIR image (e) in which it displays high signal intensity. 

Mild hydrocephalic changes are seen associated with trans-ependymal 

leak displaying high signal intensity at T2WI (d), FLAIR (e) , DWI -b0 

(f) and ADC map (i) and low signal intensity at T1WI (c) , DW-b1000 (g) 

and exponential images (h). 

Coronal (k-m) and axial (n) 3D TOF MRA show aneurysmal dilatation 

of the supraclinoid portion of the left ICA. 

Digital Subtraction angiography (o-r) shows aneurysmal dilatation of the 

supraclinoid portion of the left ICA.

- 179 - 

Illustrative cases

- 180 - 

Illustrative cases

- 181 - 

Illustrative cases

Case 19 (Fig.61):Subarachnoid hemorrhage . 

Male patient, 34 years old presented with seizors. 

- 182 - 


Axial CT examination (a-b) done 5 hours after presentation shows fresh 

blood density at the subarachnoid space mainly of the right sylvian 

fissure associated with mild hydrocephalic changes. 

MRI examination done 5 days after clinical presentation. 

The SAH shows high signal intensity at T1W images (c-d) and FLAIR 

images (g-h) and low signal intensity at T2WI (e) and Gradient (f). 

It displays low signal intensity on DWI-b0 (i), high signal intensity at 

DWI-b1000 (j) and exponential images (k) however on ADC it shows 

low signal intensity (l) as well as mild hydrocephalic changes. 

Axial 2D TOF MRA (m) shows normal flow in the right MCA without 

aneurysmal dilatation. 

Coronal 3D phase contrast MRA (n) and 3D TOF MRA (o) show 

attenuation (spasm) of the right MCA without aneurysmal dilatation. 

Digital Subtraction angiography (p-q) is normal.

- 183 - 

Illustrative cases

- 184 - 

Illustrative cases

- 185 - 

Illustrative cases

DISCUSSION 

- 186 - 

DISCUSSION 

Stroke can be defined as an acute central nervous system injury with 

an abrupt onset (Srinivasan et al.,2006). 

Stroke is a leading cause of mortality and morbidity in the developed 

world. The goals of an imaging evaluation for acute stroke are to 

establish a diagnosis as early as possible and to obtain accurate 

information about the intracranial vasculature and brain perfusion for 

guidance in selecting the appropriate therapy (Srinivasan et al.,2006). 

Although strokes are much more common in people over 65, and many 

people believe that strokes only happen to old folks, strokes can occur at 

any age, including infancy, childhood, adolescence and early adulthood 

(Caplan, 2006). 

Our study included 50 patients, 32males(64%) and 18 females(36%), 

their ages ranged from 19 to 90 years, they are classified into 8 groups 

according to their ages with 10 years interval between each group. Stroke 

patients were most commonly seen in 60-70 years age group. Their 

number were 19 patients (38%). This is followed by 50- 60 age group in 

which their number was 11 patients (22%) then 40- 50 age group in 

which their number was 8 patients (16%) and 70- 80 age group in which 

their number was 7 patients(14%). 

This result was in agreement with the study of Somay et al., 2005 

study about cerebrovacular stroke risk factors and stroke subtypes in 

different age groups included 401 patients. They were 199 males and 202 

females. The most common age groups were 71-80 and 61-70years, 

however the difference in sex prevalence between our study and their 

study may be caused by the small number of patients in our study. We are

- 187 - 

DISCUSSION 

also in agreement with Provenzale and Barboriak, 1997 regarding the 

patient age who stated that Strokes occur relatively infrequently in young 

adults (i.e., individuals who are 15-45 years old). 

The most common risk factors in our study were hypertension (15 

cases-30%), ischemic heart disease (11 cases-22%), Diabetes mellitus (9 

cases-18%) and hyperlipidemia (7 case-14%) and smoking (6 cases- 

12%).This is consistent with Somay et al., 2005 in which the 

hypertension (60.1%) was the most common risk factor followed by 

ischemic heart disease (40.1%), hypercholesterolemia (29.2%), smoking 

(31.4%) and Diabetes mellitus (21.4%) and with Eguchi et al., 2003 who 

stated that Diabetes mellitus (DM), is a major risk factor for stroke and 

also with Smoller et al., 2000 who reported that Hypertension is a major 

risk factor for stroke and heart disease among both men and women. 

The first task of imaging is to divide the strokes into ischemic (85%) 

or hemorrhagic (15%) subtypes. Distinction of hemorrhage versus 

infarction is the initial critical branch point in acute stroke triage, and 

directs care toward medical therapy or tailored intervention such as 

endovascular aneurysm coiling or thrombolysis. Hemorrhage is most 

efficiently excluded by CT, but can also be reliably assessed using MR 

imaging, which includes both T2*-weighted and FLAIR sequences 

(Rowley, 2001). 

Our patients are subjected to CT scanning then divided into two 

main groups; ischemic stroke (39 patients, 78%) and hemorrhagic stroke 

(11 patients, 22%). This is consistent with Srinivasan et al., 2006 who 

stated that acute ischemia constitutes approximately 80% of all strokes 

and is an important cause of morbidity and mortality and Haaga et al, 

2003 who said that cerebral infarction accounts for approximately 85% of

- 188 - 

DISCUSSION 

all strokes and with (Weissleder et al., 2003) who reported that 80% of 

strokes are due to cerebral ischemia. 

Temporal evolution of strokes is typically categorized into 

hyperacute (0–6 h), acute (6–24 h), subacute (24 h to approximately 2 

weeks), and chronic stroke (>2 weeks old) (Gonzalez, 2006). 

The first group, ischemic stroke patients (39 patients), are 

chronological divided into five stages. The hyperacute stage (1 st 6 hours) 

including 10 patients, the acute stage (6-24hours) including 12 patients, 

the early subacute stage(1-7 days) including 4 patients, late subacute 

stage(1-2 weeks) including 5 patients and chronic stage(>2weeks) 

including 8 cases. All these patients are subjected to different MRI 

techniques. 

Multiparametric stroke imaging combining diffusion (DWI) and 

perfusion-weighted MRI (PWI), MR angiography (MRA), and 

conventional MR sequences is increasingly used as the primary 

diagnostic imaging modality in major stroke centers (Fiehler et al, 2003). 

We had 39 ischemic stroke patients, all of them are subjected to 

conventional MRI and DWI, 37 patients are subjected to MRA, 34 

patients to MRS, 17 patient to PWI, 11 patients to Post contrast T1WI 

and only 1 case is subjected to MRV examination, however all 

hemorrhagic stroke patients are subjected to conventional MRI , DWI and 

MRA examination. 

A growing body of evidence accumulated during recent years has 

documented the superiority of magnetic resonance (MR) imaging as 

compared with computed tomography (CT) in the clinical setting of acute 

ischemic stroke not only in the diagnosis of hyperacute ischemic and 

hemorrhagic stroke but also in the proper selection of patients who might 

benefit from reperfusion therapy (Rovira et al., 2004).

- 189 - 

DISCUSSION 

Conventional computed tomography (CT) and MR imaging cannot 

be used to reliably detect infarction at the earliest time points. The 

detection of hypoattenuation on CT scans and hyperintensity on T2- 

weighted MR images requires a substantial increase in tissue water. DW 

images are very sensitive and specific for the detection of hyperacute and 

acute infarctions, with a sensitivity of 88-100% and a specificity of 86- 

100%. A lesion with decreased diffusion is strongly correlated with 

irreversible infarction (Schaefer et al., 2000). 

Diffusion-weighted MR imaging appears to be sensitive to an early 

pathoghysiologic process in cerebral infarction. The loss of adenosine 

triphosphate, which causes a subsequent shift of water from the 

extracellular space into the intracellular space and possibly an increase in 

the intracellular viscosity. 

Superior contrast-to-noise ratio (CNR) of acute stroke lesions on 

diffusion-weighted MR imaging compared with CT and conventional MR 

imaging (Gonzalez et al.,1999). 

FLAIR improved the conspicuity of ischemic lesions in comparison 

with T2 and T1, especially when lesions were located in the cortical 

ribbon were CSF contamination and different MR properties of GM can 

impair lesion conspicuity (Schaller, 2007). 

Our results are in agreement with Schaefer et al.,2000, Gonzalez et 

al.,1999 and Schaller, 2007 as we had 10 cases of hyperacute ischemic 

stroke, one case of them is diagnosed by T2WI and 9 cases not 

diagnosed. On FLAIR images 6 cases shows subtle increase of signal 

intensity and 4 cases not diagnosed however the ten cases are diagnosed 

by DWI (hyperintense with brightness). We also had 12 cases of acute 

ischemic stroke , 3 of them are diagnosed on T2WI (hyperintense ), 7 

cases showed faint hyperintensity and 2 cases not diagnosed however on

- 190 - 

DISCUSSION 

FLAIR images 11 cases are diagnosed (hyperintense) and one case not 

appear but in DWI the all 12 cases are diagnosed (hyperintense with 

brightness).These results are also in agreement with Wilcock et al., 1999 

and Karonen et al, 1999 who reported that Diffusion weighted imaging 

demonstrates changes in acute infarction before conventional T2 

weighted or CT images become positive and with Perkins et al.,2003 

who concluded that DWI nearly doubles the likelihood of detecting acute 

ischemic stroke lesions compared with FLAIR for all etiologies and in all 

anatomic locations. 

It is important to understand that DW image has T2-weighted 

contrast, the DW image can be divided by the echo-planer spin-echo T2- 

weighted (or b=0 sec/mm2) image to give an "exponential 

image"(Schaefer et al.,2000). 

A detailed understanding of the serial evolution of the brain’s MRI 

relaxation and diffusion parameters is clinically important for the 

diagnosis and treatment of stroke patients. For example, it can be used to 

help estimate the age of a lesion, to establish rational time windows for 

stroke treatment, or perhaps to provide alternative outcome measures or 

“surrogate end points (Liu et al, 2007). 

In humans, decreased diffusion in ischemic brain tissue is observed 

as early as 30 min after vascular occlusion. The ADC continues to 

decrease with peak signal reduction at 1–4 days. This decreased diffusion 

is markedly hyperintense on DWI (a combination of T2 and diffusion 

weighting), less hyperintense on exponential images, and hypointense on 

ADC images. The ADC returns to baseline at 1–2 weeks. This is 

consistent with the persistence of cytotoxic edema (associated with

- 191 - 

DISCUSSION 

decreased diffusion) as well as cell membrane disruption, and the 

development of vasogenic edema (associated with increased diffusion). 

At this point, a stroke is usually mildly hyperintense on the DWI images 

due to the T2 component and isointense on the ADC and exponential 

images. Thereafter, the ADC is elevated secondary to increased 

extracellular water, tissue cavitation, and gliosis. There is slight 

hypointensity, isointensity or hyperintensity on the DWI images 

(depending on the strength of the T2 and diffusion components), 

increased signal intensity on ADC maps, and decreased signal on 

exponential images (Gonzalez et al., 2006). 

This is consistent with our study as we found decreased ADC in 

the hyperacute stage with more decrease in the acute stage and it started 

to increase to reach near normal levels in the late subacute stage with 

more increase in the chronic stage, by other means the rADC (ratio 

between ADC in infarction and contralateral normal site) is 0.5308± 

0.0899 in the hyperacute, 0.3765± 0.06954 in the acute stage, 0.7002± 

0.1231in the early subacute, 1.0135± 0.03422 in late subacute and 

2.2094± 0.8806 in chronic stage. 

In our study, we found that patients with hyperacute stroke (in the 

first 6 hours-10 patients) the infarction could be visualized in DWI b 

1000 (hyperintensity with brightness), ADC map (hypointensity) and 

exponential images (hyperintensity) however 9 patients couldn’t be seen 

on the DWI b0 or T2-wieghted image . In the FLAIR 4 patients out of 

them were not appear completely while the remaining 6 patients showed 

slight intensity. 

Patients with acute stroke (6-24 hours-12 patients) the infarction 

could be visualized in DWI b 1000 (hyperintensity with brightness), ADC 

map (hypointensity) and exponential images (hyperintensity) however on

- 192 - 

DISCUSSION 

the DWI b0 and T2-wieghted image 2 patients couldn’t be seen, 7 cases 

showed faint hyperintensity and 3 patients are hyperintense . In the 

FLAIR 1 patients out of them was not appear completely while the 

remaining 11 patients showed hyperintensity. 

This is consistent with Schaefer et al., 2000 who observed 

restricted diffusion associated with acute ischemia 30 minutes after a 

witnessed ictus. The ADC continues to decrease and is most reduced at 8- 

32hours. The ADC remains markedly reduced for 3-5 days. This 

decreased diffusion is markedly hyperintense on DW images and 

hypointense on ADC images and with Yang et al, 1999 who reported that 

acute infarcts appear hyperintense on DWI because of a reduction in the 

apparent diffusion coefficient (ADC) of water within minutes after the 

onset of ischemia. We are also in agreement with Keir and Wardlaw, 

2000 who stated that DWI works on the principle that sensitizing a 

standard MR image to diffusion weighting identifies regions of abnormal 

water movement, occurring very early after onset of ischemia, resulting in 

increased (bright) signal intensity. This is consistent also with Neumann- 

Haefelin et al 1999 and Krueger et al, 2000 who reported that with DWI 

it is possible to identify severely ischemic brain regions within minutes to 

hours after stroke onset. A decrease in the apparent diffusion coefficient 

of water (ADC), apparent as hyperintensity on DW images, indicates a 

restriction in the diffusional movement of water. 

In our study patients with early subacute stroke (1-7 days-4 

patients) showed hyperintensity in DWI (b1000 and b0),exponential 

image, T2-weighted and FLAIR images but hypointensity on ADC maps. 

Patients with late subacute stroke (1-2 weeks-5 patients) showed 

hyperintensity in DWI (b1000 and b0), T2-weighted and FLAIR images 

and isointense signal at exponential image and ADC maps.

- 193 - 

DISCUSSION 

Chronic stroke patients (>2weeks-8 patients) showed hyperintensity 

on T2-weighted, FLAIR images and DWI ( b0).On DWI ( b1000) 6 cases 

showed hyperintensity however 2 cases were isointense. The all 8 cases 

were hyperintense on ADC maps. 

These agree with Schaefer et al.,2000 who said that the ADC 

returns to baseline at 1-4 weeks. This most likely reflects persistence of 

cytotoxic oedema(associated with decreased diffusion) and development 

of vasogenic oedema and cell membrane disruption, leading to increased 

extracellular water (associated with increased diffusion). At this point, an 

infarction is usually mildly hyperintense due to the T2 component on DW 

images and isointense on the ADC images. Thereafter, diffusion is 

elevated as a result of continued increase in extracellular water, tissue 

caviation and gliosis. This elevated diffusion is characterized by slight 

hypointensity, isointensity or hyperintensity on DW images (depending 

on the strength of the T2 and ADC maps. 

These also agree with Huang et al., 2001 who reported that when 

the signal intensity changes on DW images were studied as a single 

parameter, abnormally high signal intensity was constantly observed at 

the acute and the subacute stages of cerebral infarction. This abnormal 

signal intensity increased with time and declined 2 weeks after symptom 

onset. Lansberg et al., 2001 also reported that it is well accepted that 

ADC values decline rapidly after the onset of ischemia and subsequently 

increase, the observed time course of the ADC increase to supernormal 

values has varied from 24 hours to 17 days. 


irreversibly infarcted tissue (Srinivasan et al, 2006), perfusion imaging 

findings provide information on the momentary hemodynamic state of 

brain tissue, as they reveal impaired tissue perfusion caused by blood

- 194 - 

DISCUSSION 

vessel obstruction. Therefore, perfusion imaging findings may yield 

information about pathologically hypoperfused regions, even before 

genuine structural brain tissue damage has taken place (Wittsack et al, 

2002). 

Perfusion-weighted imaging (PWI) and diffusion weighted imaging 

(DWI) have been used with increasing frequency in acute ischemic 

stroke. PWI demonstrates areas of decreased blood flow, whereas DWI 

reveals regions of acute bioenergetic compromise ( Loh et al, 2005). 

The combination of DW imaging, perfusion- weighted imaging, and 

MR angiography enables identification of tissue at risk of infarction, 

which is characterized by the mismatch between an area of restricted 

diffusion and a larger area with ischemic but still viable tissue on 

perfusion-weighted images (Saur et al., 2003). 

A variety of hemodynamic images may constructed from perfusion 

data, including relative cerebral blood volume(rCBV), relative cerebral 

blood flow(rCBF), mean transit time (MTT)and time to peak (TTP) maps 

(Schaefer et al.,2000). 

Cerebral blood volume (CBV) is defined simply as the amount of 

blood in a given amount of tissue at any time (ml/g) as compared to CBF, 

which represents the amount of blood moving through a certain amount 

of tissue per unit time (ml/g per min). The ratio of CBV and CBF is 

defined as the mean transit time (units minutes) (Davis et al, 2003). Time 

to peak (TTP) maps of perfusion imaging show the arrival time of the 

contrast agent which is the same for the gray and white matter in the brain 

(Wittsack et al., 2002). 

In our study we used MTT and TTP maps for the correlation 

between the lesion size on perfusion weighted images and its size on DW 

images.

- 195 - 

DISCUSSION 

It is difficult to name one perfusion map type that could, even when 

combined with DW images, be used to predict infarct growth with 

satisfactory accuracy. Although the initial lesion volume on rCBV maps 

correlates best with the final infarct size and on average is closest to it, 

the initial rCBV map in many patients lead to underestimation of the final 

infarct size. Estimating the final infarct size with the initial rCBF finding 

seems to be more accurate. However, some infarcts grow to the area 

where the only initially detected imaging abnormality is prolonged MTT 

(Karonen et al., 2000). 

In an acute stroke setting, TTP maps offer two advantages over 

other images derived from perfusion imaging. First, they involve the least 

amount of post processing, and thus allows the clinical information to be 

available within 20 minutes. Second, TTP maps provide a relatively clear 

picture of the location and extent of the lesion (Wittsack et al., 2002). 

The volume of sever ischemia determined at a TTP delay of some 6 

seconds relative to the non affected hemisphere helped to predict the 

definite infarct lesion (Seitz et al.,2005). 

When most patients of hyperacute and acute infarction are evaluated 

by DW and perfusion-weighted MR imaging, their images usually 

demonstrate one of three patterns: A lesion is smaller on DW images than 

the same lesion on perfusion –weighted image; a lesion on DW images is 

equal to or larger than that on perfusion weighted images; or a lesion is 

depicted on DW images but not demonstrable on perfusion-weighted 

images (Schaefer et al.,2000). 

Schaefer et al.,2000 found that the large-vessel stroke lesion (such 

as in the proximal portion of the middle cerebral artery), the abnormality 

as depicted on perfusion-weighted images is frequently larger than the 

lesion as depicted on DW images, the peripheral region characterized by

- 196 - 

DISCUSSION 

normal diffusion and decrease perfusion, usually progress to infarction 

unless there is early reperfusion. Thus, in the acute setting, perfusion- 

weighted imaging in combination with DW imaging helps identify an 

operational "ischemic penumbra" or area at risk for infarction. 

On the other hand, with small-vessel infarction (perforator 

infarctions and distal middle cerebral artery infarctions) the initial lesion 

volumes on perfusion-weighted and DW images are usually similar, and 

the DWI lesion volume increases only slightly with time. A lesion larger 

on DW images than on perfusion weighted images or a lesion visible on 

DWI but not on perfusion weighted images usually occurs with early 

reperfusion. In this situation, the lesion on DW images usually does not 

change substantially over time. 

These are in agreement with our results as 8 patients of hyperacute 

and acute stroke in our series showed PWI> DWI, 7 patients of them 

were suffering from lesions in the distribution of large cerebral blood 

vessels . 6 patients of hyperacute, acute and chronic stroke showed 

DWI=PWI , their lesion were in the distribution of small vessels. 2 

patients showed DWI>PWI , and 1 patient showed lesion visible on DWI 

but not on perfusion weighted images ,their lesion were in the distribution 

of small vessels with reperfusion. 

These are also in agreement with Gonzalez et al., 2006 who stated that 

Proximal occlusions are much more likely to result in a diffusion– 

perfusion mismatch than distal or lacunar infarctions and with Neumann- 

Haefelin et al, 2000 who concluded that the total PWI/DWI mismatch is 

often larger in patients with ipsilateral carotid stenosis .70% than in 

patients without carotid stenosis.

- 197 - 

DISCUSSION 

In cases with diffusion perfusion mismatch and ischemic penumbra we 

found increase in the MTT and delay in TTP in the penumbra region 

compared with the normal contralateral site (MTT at the penumbra is 

17.6250± 2.7675 sec and 10.6000± 2.8087 sec at normal site, TTP at the 

penumbra is 44.7875± 12.1561sec and 35.9375± 11.2246 sec at normal 

site) denoting statistically significant difference between ischemic and 

contralateral normal site, p

- 198 - 

DISCUSSION 

the more distal, smaller branches and the level of diagnostic confidence 

diminishes (Davis et al, 2003). 

In acute stroke imaging (

- 199 - 

DISCUSSION 

marked vascular enhancement was observed in 2 patients of hypercaute 

stroke however mild enhancement was detected in 3 patients [ 2 cases of 

hyperacute stroke and 1 case of acute stroke] .So vascular enhancement 

was noted in hyperacute and acute stages not the chronic stages and this 

is consistent with Gonzalez et al., 2006. 

Magnetic Resonance Spectroscopy (MRS) has become one of the 

most important imaging techniques of CNS over 10 years, mainly 

because this method is enables noninvasive measurement of metabolites 

which play a central role in cellular metabolism (Kaminska et al, 2007). 

MRS has been suggested to be more sensitive than MRI in detecting 

hypoxic damage. It has been proposed that MRS may be able to detect 

cerebral ischemia within seconds of its onset as compared to DWI that 

provides warning as early as 1 h after the onset. The most striking 

changes in patients with acute cerebral infarction on MRS is the 

appearance of lactate with reduction in NAA and total Cr/PCr within the 

infarct compared to the contralateral hemisphere. Large variations in the 

initial concentrations of Cho have been observed in the region of 

infarction (Davis et al, 2003). 

34 cases of ischemic stroke patients are subjected to MR 

spectroscopic examination to the lesion (infarction) and the contralateral 

normal area (10 patients of hyperacute stroke, 10 patients of acute stroke, 

6 patients of subacute stroke and 8 patients of chronic stroke). 

Lactate is not normally detected within the brain and, as the end 

product of glycolysis, is a particularly useful measure of metabolism. The 

concentration of lactate rises when the glycolysis rate exceeds the tissue's 

capacity to catabolise it or remove it from the blood stream. The rise in 

brain lactate that results from the mismatch between glycolysis and 

oxygen supply, making it the hallmark for the detection of cerebral

- 200 - 

DISCUSSION 

ischemia. The persistence of lactate weeks or months following stroke 

onset has been observed. Removal of lactate depends on tissue perfusion, 

the permeability of the blood brain barrier (BBB) and diffusion of the 

metabolite through the damaged tissue (Saunders, 2000 ). 

In our study the lactate is present in all hyperacute(100%), 

acute cases(100%), 3 cases of early subacute(75%) , 1 cases of late 

subacute(50%) and 4 cases of chronic stroke(50%) with statistical 

significant difference in lactate level among different stroke stages 

(p

- 201 - 

DISCUSSION 

This is consistent with our study as all our patients in different stroke 

stages showed decrease in the level of NAA. We also in agreement with 

Graham et al, 2001, Pereira et al, 1999, Mathews et al., 1995, , Graham 

et al,1993 and Graham et al, 1992 who observed that lnfarcts were 

characterized by significantly increased lactate and significantly 

decreased NAA compared with contralateral brain regions. Our study is 

consistent with Gideon et al, 1992 who concluded that the NAA content 

in infarcted brain tissue is considerably reduced compared with normal 

brain tissue. 

Initial reductions in Cr/PCr are identified following infarction and 

further reductions have been demonstrated up to 10 days following the 

time of onset. The pathological correlate is thought to be gliosis of the 

tissue. The reduction in NAA in the infarct region is more marked than 

the reduction in Cr/PCr and this is thought to reflect the increased 

sensitivity of neurons to ischemia, compared to glial tissue (Davis et al, 

2003) and (Saunders, 2000 ). 

These are consistent with our study as 28 patients showed reduction 

in Cr/PCr and 6 patients were normal or showed slight increase of Cr/PCr 

level. 

The trimethylamine resonance of choline-containing compounds is 

present at 3.22 ppm. In normal brain, the Cho peak is thought to consist 

predominantly of glycerolphosphocholine and phosphocholine. 

Both compounds are involved in membrane synthesis and degradation. 

Reduction in the choline peak has been proposed as a marker of 

membrane damage. The choline peak has been shown to be increased, 

decreased and stays the same following cerebral infarction. The changes 

in the choline peak are thought to reflect changes in the MR visibility of 

the choline containing compounds that make up the cell membrane. We

- 202 - 

DISCUSSION 

have shown a fall and then a late rise, maximal 3 months after onset of 

stroke. This may represent loss of membrane function, followed by late 

gliosis (Davis et al, 2003). 

In our study the choline level was decreased in 22 out of 26 cases of 

early ischemic stroke (hyperacute, acute and subacute stages) however in 

chronic stage choline level is increased in 4 cases and decreased in 4 

cases. 

When comparing MRS findings in different ischemic stroke stages we 

found that there is a statistical significant difference in NAA level among 

different stroke stages(p

- 203 - 

DISCUSSION 

extension, 2 cases of subarachnoid hemorrhage and 1 case of 

intraventricular hemorrhage . 

The ability to detect acute hemorrhage by MRI is related to the 

oxygen saturation of hemoglobin and its degradation. As a hematoma 

ages, the hemoglobin passes through several forms (oxyhemoglobin, 

deoxyhemoglobin, and methemoglobin) prior to red cell lysis and 

breakdown into ferritin and hemosiderin (Davis et al, 2003). 

Based on the most mature form of the hemoglobin present in the clot, 

five stages of evolving ICH have been described. The hyperacute stage 

lasts for 24 h, acute stage for 2–3 days, early subacute stage for 3–7 days, 

late subacute stage up to 2 weeks and chronic stage more than 2 weeks. 

The evolution of an ICH is a complex and dynamic process and the 

estimation of the time of onset based on MRI findings may be inaccurate 

(Kummer and Back, 2006). 

It was initially believed that on MRI an ICH of less than 24 h 

duration could not be distinguished reliably either from a mass lesion or 

from an acute infarct, because of an unspecific pattern of isointensity in 

T1 and slight hyperintensity on T2 imparted by the predominance of 

oxyhemoglobin. However, due to a reduced oxygen tension at the 

periphery of the clot, some deoxygenation of hemoglobin occurs 

immediately after the bleeding, and several studies have demonstrated 

that the resulting susceptibility effects can be visualized very early on T2- 

and particularly on T2*-weighted images as a hypointense rim . It was 

reported that the ability of high field MRI to reliably detect a spontaneous 

ICH as early as 20 min after onset and schematized the appearance of the 

hyperacute hemorrhage as consisting of three distinct concentric regions. 

The center of the hemorrhage appears isointense or heterogeneously 

hyperintense on T2- and T2*-weighted images, probably reflecting the

- 204 - 

DISCUSSION 

presence of intact oxyhemoglobin. The periphery is hypointense on T2- 

and T2*-weighted images reflecting the susceptibility effects due to 

deoxyhemoglobin, and finally there is an outer rim that appears 

hypointense on T1-weighted images and hyperintense on T2- and T2*- 

weighted images, suggestive of edema (Kummer and Back, 2006). 

Diffusion MR data would differ among the stages of evolving 

hematomas in that hematomas containing blood with intact cell 

membranes would have restricted diffusion compared with those 

hematomas in which RBC membranes have lysed. This hypothesis was 

based on several facts. First, the presence of intact cell membranes 

restricts molecular diffusion (Atlas et al, 2000). 

Results of DW imaging of hematomas at this stage have not been 

well characterized; however a hyperacute intraparenchymal hemorrhage 

is hyperintense on DW images, with a decreased apparent diffusion 

coefficient (ADC). The possible causes for the decreased ADC are 

shrinkage of the extracellular space due to clot retraction, changes in the 

concentration of hemoglobin and a high viscosity (Moritani et al, 2005). 

These are consistent with our study as we had 2 cases of hyperacute 

hemorrhagic stroke. At conventional MRI the lesions showed 

intermediate signal intensity at T1, slightly high signal intensity at T2WI, 

FLAIR and Gradient images. The periphery of the lesions showed low 

signal intensity at T2WI, FLAIR and Gradient (T2*) images. On DW 

images the lesions showed high signal intensity (restricted diffusion) and 

low signal intensity on ADC maps. We are also in agreement with 

Linfante et al, 1999 who reported that hyperacute hematomas have 

increased signal intensity present on FLAIR and T2WI, and the 

hypointensity present on T1WI and with Fiebach et al, 2004 and Patel 

et al, 1996 who concluded that Intracranial hemorrhage less than 24 hours

- 205 - 

DISCUSSION 

old has been postulated to be in the oxyhemoglobin phase and would be 

isointense on T1-weighted images and slightly hyperintense on T2- 

weighted images, with additional feature in all the cases is a peripheral 

rim of hypointensity on both T1- and T2-weighted images. 

In the absence of rebleeding, deoxygenation of the clot is completed 

in most cases by 24 h. At that time deoxyhemoglobin becomes the 

predominant blood breakdown product in the lesion. Due to its 

paramagnetic properties and its compartmentalization within still intact 

RBCs, deoxyhemoglobin exerts a strong susceptibility effect, which 

makes acute hematomas appear distinctly and characteristically dark on 

T2 weighted SE images, and more so on T2* weighted GRE images . On 

T1-weighted images, acute ICHs still appear isointense or mildly 

hypointense, as in the hyperacute stage. The parenchyma surrounding the 

clot exhibits a halo due to vasogenic edema and initial inflammatory 

reaction. The region of edema has long T1 and T2 relaxation times and 

appears hypointense on T1-weighted images and hyperintense on T2- 

weighted images (Kummer and Back, 2006). 

Diffusion-weighted images of an acute hematoma show a marked 

hypointensity, caused by the magnetic field inhomogeneity created by the 

para-magnetic deoxy-hemoglobin. Although The ADC has been reported 

to be decreased, accurate calculations are often difficult (Moritani et al, 

2005). 

These is consistent with our results as we had 2 cases of acute 

intracerebral hematomas. At T1WI they showed intermediate signal 

intensity with hyperintense peripheral rim however at they showed low 

signal intensity at T2-weighted, FLAIR and Gradient images. They 

showed low signal intensity on DW images and ADC maps.

- 206 - 

DISCUSSION 

This is also in agreement with Schaefer et al.,2000 who reported 

that hemorrhage containing deoxyhemoglobin, intracellular 

methemoglobin and hemosiderin and hypointense on DW images because 

of magnetic susceptibility and with Kang et al., 2001 who observed that 

all acute hemorrhagic cases showed marked hypointensity on DW, T2- 

weighted, FLAIR and Gragient images. We are also in agreement with 

Schellinger et al, 1999 who concluded that the key substrate for MRI 

visualization of hemorrhage is deoxyhemoglobin, which causes a signal 

loss in T2-weighted imaging (T2-WI) because of paramagnetic 

susceptibility effects, although usually not within the first 12 to 24 hours. 

The appearance of methemoglobin in the clot marks the transition 

from the acute to the subacute phase. In the early subacute phase, 

methemoglobin is still compartmentalized within red blood cells and 

hence generates local field gradients that maintain a T2 shortening effect 

similar to that induced by deoxyhemoglobin. Therefore, in the early 

subacute phase relaxivity effects and susceptibility effects coexist, i.e. the 

clot appears bright in T1, and dark in T2 and especially in T2*. This stage 

is expected to last for approximately 1 week (Kummer and Back, 2006). 

On DW imaging, intracellular met-hemoglobin shows hypointensity 

due to paramagnetic susceptibility effects and ADC measurements are not 

reliable due to susceptibility effects (Moritani et al, 2005). 

In our study we had 1case of early subacute hemorrhage. The case 

showed high signal intensity on T1, low signal intensity at T2-weighted, 

FLAIR and Gradient images. The patient showed low signal intensity on 

DW images and ADC maps. 

This is consistent also with Kang et al., 2001 who observed that all 

early subacute hemorrhagic cases showed marked hypointensity on DW, 

T2-weighted, FLAIR and Gradient images and with Schaefer et al.,2000

- 207 - 

DISCUSSION 

who reported that hemorrhage containing deoxyhemoglobin, intracellular 


of magnetic susceptibility. 

As the clot ages, progressive fragmentation and osmotic phenomena 

damage RBC membranes until they eventually lyse. Hemolysis releases 

methemoglobin into the extracellular fluid compartment of the 

hematoma. The resulting dilution of methemoglobin in the extracellular 

fluids eliminates the biological field gradients, and with them the 

susceptibility phenomena, an effect that is observed initially at the 

periphery of the clot. When all methemoglobin is extracellular, the T2- 

shortening induced signal loss is no longer observed, so that the late 

subacute ICH is predominantly hyperintense in both T1- and T2-weighted 

images (Kummer and Back, 2006). 

It has been reported that late subacute hematomas are hyperintense 

on DW imaging. The ADC value for the late subacute hematoma is 

controversial (Moritani et al, 2005). 

Extracellular methemoglobin has a higher ADC than does normal 

brain tissue, which indicates that the mobility of water in the extracellular 

space is increased. The prolongation of the T2 component of fluid with 

extracellular methemoglobin results in hyperintensity on DW images 

(Schaefer et al.,2000). 

This is consistent with our study as we had 2 cases of late subacute 

hematoma that showed hyperintense signal at T1, T2, FLAIR , Gradient , 

DW images and ACD maps. 

We are in agreement with Kang et al., 2001 who observed that all 

cases of late subacute hematomas showed marked hyperintensity at 

diffusion-weighted, T1-, T2-weighted and FLAIR images.

- 208 - 

DISCUSSION 

A chronic ICH initially shows a hypointense peripheral hemosiderin 

rim completely surrounding a central area hyperintense in all sequences 

due to the persistence of extracellular methemoglobin. The hemosiderin 

rim is less conspicuous on T1-weighted sequences and more conspicuous 

on T2- and T2*-weighted sequences (Kummer and Back, 2006). 

Diffusion-weighted images are hyperintense in chronic hematomas. 

The ADC value has been reported to be increased, but this is often 

difficult to measure accurately due to paramagnetic susceptibility artifacts 


Hemorrhage containing deoxyhemoglobin, intracellular 


of magnetic susceptibility (Schaefer et al.,2000). 

We are in agreement with Kummer and Back, 2006 and Schaefer et 

al.,2000 as we had 1 case of chronic intracerebral hematoma. It showed 

low signal intensity with small high signal intensity center at T1-, T2- 

weighted, FLAIR and Gradient images. It showed low signal intensity on 

DW images with increased ADC value. 

Subarachnoid Hemorrhage (SAH) is responsible of 3% of all acute 

strokes and of 5% of stroke-related deaths. Rupture of intracranial 

saccular aneurysm accounts for about 85% of cases of SAH (Kummer 

and Back, 2006). 

Ninety per cent of non-traumatic SAHs are caused by ruptured 

Berry aneurysms ( Howlett and Ayers, 2004). 

Our results are in agreement with Kummer and Back, 2006 and 

Howlett and Ayers, 2004 as we had 2 cases of subarachnoid hemorrhage 

4 % (out of 50 patients with stroke). One of them is caused by rupture of 

intracranial aneurysm (50%). The difference in incidence of ruptured

- 209 - 

DISCUSSION 

intracranial aneurysms as a causative factor is due to the small number of 

SAH cases in our study. 

Conventional T1–WI and T2–WI were shown to be ineffective in 

the diagnosis of acute SAH. The detection of SAH may be improved by 

using PD–WI with shorter repetition times (TR) to visualize the T1- 

effect. FLAIR sequences have been reported to be suitable for the 

diagnosis of not only subacute but also acute SAH (Davis et al, 2003). 

We are in agreement with Davis et al, 2003 as Our 2 cases were 

subacute. On case was detected by all pulse sequences, however the other 

case was detected by FLAIR images only. 

It is often difficult to detect subarachnoid hemorrhage on DW 

images. However, DW images may be useful to visualize parenchymal 

injuries secondary to subarachnoid hemorrhage. Ischemic changes, 

probably related to subarachnoid hemorrhage, have shown hyperintensity 

on DW images (Moritani et al, 2005). 

Most intraventricular hemorrhages (IVHs) are secondary to ICH or 

SAH. Isolated IVH is rare and usually due to the rupture of underlying 

vascular malformations. Since the CSF in ventricles has a higher content 

in oxygen and glucose, the layered form evolves more slowly compared 

to the clotted form. The latter evolves at a rate similar to ICH. However, 

in the chronic stage, unlike ICH, IVHs do not show hemosiderin 

formation. Among the conventional sequences, proton density depicts 

IVH better than T1- and T2-weighted images. In the acute stage FLAIR 

may have better sensitivity than CT scan to demonstrate IVH. On FLAIR, 

in the initial 48 h IVH appears hyperintense (Kummer and Back, 2006). 

DW images can demonstrate intraventricular hemorrhages, but in general 

the GRE images have a higher sensitivity (Moritani et al, 2005).

- 210 - 

DISCUSSION 

We had 2 cases of intraventricular hemorrhage. One of them is 

associated with hyperacute intracerebral hematoma and showed the same 

signal intensity. The other case was acute and showed intermediate signal 

intensity at T1 and low signal intensity at all other pulse sequences. 

MR angiography has recently been established as a valid and 

sensitive tool to demonstrate pathologic findings in extra- and intracranial 

arteries in acute stroke (Seitz et al, 2005). 

Magnetic resonance angiography (MRA) was done to all our 

hemorrhagic stroke cases (11 patients), 5 patients showed positive finding 

[spasm in 2 cases and non filling in 1 case of intracerebral hematoma – 

aneurysm in 1 case and spasm in 1 case of SAH]. 

The presence of a significant quantity of blood in the brain disrupts 

the homogeneity of the magnetic field due to the presence of the iron 

from the hemoglobin molecule, and spectroscopy cannot be carried out in 

patients with large intracerebral hemorrhages (Davis et al, 2003). So MR 

spectroscopic study was not included in our hemorrhagic stroke cases.

Summary and Conclusion 

- 211 - 

Summary& Conclusion 

Despite the efforts being made to develop effective treatments, 

ischemic stroke remains a common cause of death and disability in the 

industrialized world. It has been claimed that new imaging methods could 

provide valuable information in developing new therapies. 

Any magnetic resonance (MR) imaging protocol for acute ischemic 

stroke must be able to depict early ischemic changes in a sensitive manner. 

This can be achieved with diffusion-weighted (DW) and perfusion- 

weighted (PW) MR imaging. DW MR imaging depicts infarcted tissue 

within 5 minutes after the occlusion of the feeding vessel. PW imaging is 

able to depict hypoperfused brain tissue around the infarcted core. The 

mismatch between lesion sizes at PW and DW imaging (perfusion-diffusion 

mismatch) in the acute phase has been considered as an estimate of the 

ischemic penumbra and is helpful in selecting patients for different 

treatment groups (Karonen et al.,2000). 

Our study included 50 patients, 32males (64%) and 18 females (36%), 

their ages ranged from 19-90 with mean age 59.6±14.1 years. The most 

common risk factors in our study were hypertension (15 cases-30%) 

followed by ischemic heart disease (11 cases-22%). 

Our patients are divided into two main groups; ischemic stroke (39 

patients, 78%) and hemorrhagic stroke (11 patients, 22%). 

The first group, ischemic stroke patients (39 patients), are 

chronological divided into five stages. The hyperacute stage (1 st 6 hours) 

including 10 patients, the acute stage (6-24hours) including 12 patients, the 

early subacute stage (1-7 days) including 4 patients, late subacute stage(1-2

- 212 - 


weeks) including 5 patients and chronic stage(>2weeks) including 8 cases. 

All these patients are subjected to different MRI techniques. 

On DWI we found decreased ADC in the hyperacute stage with 

more decrease in the acute stage and it started to increase to reach near 

normal levels in the late subacute stage with more increase in the 

chronic stage. 

Most of hyperacute and acute ischemic stroke patients (17 patients) 

were evaluated by perfusion weighted images (PWI). We used MTT and 

TTP maps for the correlation between the lesion size on perfusion weighted 

images and its size on DW images. 

Eight (8) patients of hyperacute and acute stroke in our series showed 

PWI> DWI, 7 patients of them were suffering from lesions in the 

distribution of large cerebral blood vessels . 6 patients of hyperacute, acute 

and chronic stroke showed DWI=PWI , their lesion were in the distribution 

of small vessels. 2 patients showed DWI>PWI , and 1 patient showed lesion 

visible on DWI but not on perfusion weighted images ,their lesion were in 

the distribution of small vessels with reperfusion. 

Postcontrast T1 was done in 11 patients. Vascular enhancement was 

positive in 5 patients out of them. Vascular enhancement was noted in 

hyperacute and acute stages not the chronic stages. 

Thirty four (34) cases of ischemic stroke patients are subjected to MR 

spectroscopic examination. Lactate was present in all hyperacute, acute 

cases, and most of subacute and chronic stages. Decrease in the level of 

NAA in all our patients in different stroke stages, reduction in Cr/PCr in 

most patients and varied level of choline amoung patients.

- 213 - 


Our study included 11 patients of hemorrhagic stroke, they were 8 

cases with intracerebral hemorrhage; one of them showed intraventricular 

extension, 2 cases of subarachnoid hemorrhage and 1 case of 

intraventricular hemorrhage. 

We had 2 cases of hyperacute hemorrhagic stroke. At conventional 

MRI the lesions showed intermediate signal intensity at T1, slightly high 

signal intensity at T2WI, FLAIR and Gradient images. The periphery of the 

lesions showed low signal intensity at T2WI, FLAIR and Gradient (T2*) 

images. On DW images the lesions showed high signal intensity and low 

signal intensity on ADC maps. We had also 2 cases of acute intracerebral 

hematomas. At T1WI they showed intermediate signal intensity with 

hyperintense peripheral rim however at they showed low signal intensity at 

T2-weighted, FLAIR and Gradient images. They showed low signal 

intensity on DW images and ADC maps. We had 1case of early subacute 

hemorrhage. The case showed high signal intensity on T1, low signal 

intensity at T2-weighted, FLAIR and Gradient images. The patient showed 

low signal intensity on DW images and ADC maps. We had 2 case of late 

subacute hematoma that showed hyperintense signal at T1, T2, FLAIR, 

Gradient, DW images and ACD maps. We had 1 case of chronic 

intracerebral hematoma. It showed low signal intensity with small high 

signal intensity center at T1-, T2- weighted, FLAIR and Gradient images. It 

showed low signal intensity on DW images with increased ADC value. 

We had 2 cases of subarachnoid hemorrhage 4 % (out of 50 patients 

with stroke). One of them is caused by rupture of intracranial aneurysm 

(50%). Our 2 cases were subacute. On case was detected by all pulse 

sequences, however the other case was detected by FLAIR images only. 

We had 2 cases of intraventricular hemorrhage. One of them is 

associated with hyperacute intracerebral hematoma and showed the same

- 214 - 


signal intensity. The other case was acute and showed intermediate signal 

intensity at T1 and low signal intensity at all other pulse sequences. 

MRA showed positive data in 5 out of 11 patients. 

Conclusion: 

*Diagnosis of ischemic stroke has been improved by the use of magnetic 

resonance(MR) imaging. 

*Diffusion Weighted Images (DWI) is superior to CT and conventional 

MRI sequences in early detection of hyperacute and acute ischemic stroke. 

*The combination DWI with Perfusion Weighted Images (PWI) enables 

identification of tissue at risk of infarction which is characterized by the 

mismatch between an area of restricted diffusion and a larger area with 

ischemic but still viable tissue on perfusion-weighted images. 

* MRA can pinpoint the cause of infarction mainly in large proximal 

vessels than distal smaller ones more in hyperacute and acute ischemic 

stages. 

*Contrast-enhanced T1-weighted images can show arterial enhancement in 

hyperacute and strokes due to slow or collateral flow. 

*The most striking changes in patients with cerebral infarction on MRS is 

the appearance of lactate with reduction in NAA and total Cr/PCr with 

variations in the concentrations of Cho. 

*Initial CT is important in early cases of stroke to diagnose Intracranial 

hemorrhage. 

*Based on the most mature form of the hemoglobin present in the clot, five 

stages of evolving ICH have been described. Each has specific appearance 

on conventional MRI and DW images. 

*MR angiography is a sensitive tool to demonstrate pathologic findings in 

extra- and intracranial arteries in hemorrhagic stroke as occlusion, spasm or 

intracranial aneurysms.

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- 1 - 

ﻲﺑﺮﻌﻟا ﺺﺨﻠﻤﻟا 

يدﺆﺗ ﻰﺘﻟا بﺎﺒﺳﻷا ﻢهأ ﻦﻣ ﺮﺒﺘﻌﺗ ﺎﻤآ تﺎﻴﻓﻮﻟا بﺎﺒﺳأ ﻢهأ ﻦﻣ ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا ﺮﺒﺘﻌﺗ 

راﺮﻘﻟا ﺬﺧأ ﻦﻣ ﻦﻜﻤﺘﻠﻟ تﻻﺎﺤﻟا ﻩﺬﻬﻟ 

ﺮﻜﺒﻤﻟا ﺺﻴﺨﺸﺘﻟا ةروﺮﺿ ﺐﺟﻮﺘﺴﻳ ﺎﻤﻣ ﺮﻀﺤﺘﻤﻟا ﻢﻟﺎﻌﻟا ﻲﻓ 

ﺦﻤﻟا ﻦﻣ ءﺰﺟ ﻰﻟا ﺔﻳﻮﻣﺪﻟا ةروﺪﻟا ﻲﻓ رﻮﺼﻗ 

ﻦﻋ ﺔﺠﺗﺎﻧ تﻻﺎﺣ 

ﻰﻟإ 

. جﻼﻌﻟا ﺔﻘﻳﺮﻃ ﻦﻋ ﺢﻴﺤﺼﻟا 

ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا تﻻﺎﺣ ﻢﺴﻘﻨﺗ 

. ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا ﻦﻋ ﺔﺠﺗﺎﻧ تﻻﺎﺣ وأ 

و ﺎﻬﺘﻟﻮﻬﺴﻟ رﺎﺸﺘﻧﻻا ﻊﺳاو ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا ﺺﻴﺨﺸﺗ ﻲﻓ ﺔﻐﺒﺻ نوﺪﺑ ﺔﻴﻌﻄﻘﻤﻟا ﺔﻌﺷﻷا ماﺪﺨﺘﺳا نإ 

رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا تﻻﺎﺤﻟا ﺾﻌﺑ ﻰﻟإ 

ﺔﻓﺎﺿﻻﺎﺑ ﻒﻳﺰﻨﻟا تﻻﺎﺣ ﺺﻴﺨﺸﺗ ﻦﻣ ﺎﻨﻜﻤﺗ ﺚﻴﺣ ﺎﻬﺘﻋﺮﺳ 

مﺪﻋو 

تﻻﺎﺤﻟا ﻢﻈﻌﻤﻟ ﺮﻜﺒﻤﻟا ﺺﻴﺨﺸﺘﻟا ﻲﻓ ﺎﻬﺘﻴﺳﺎﺴﺣ مﺪﻋ ﺎﻬﺑﻮﻴﻋ 

ﻦﻣ ﻦﻜﻟ و ﺔﻳﻮﻣﺪﻟا 

ةروﺪﻟا ﻲﻓ 

. ﺔﺑﺎﺻﻹا 

ﻢﺠﺣ ﺪﻳﺪﺤﺗ ﻲﻓ ﺔﻗﺪﻟا مﺪﻋ و ةﺮﻴﻐﺼﻟا تﺎﺑﺎﺻﻹا 

ﺾﻌﺑ رﺎﻬﻇإ 

ﻰﻠﻋ ةرﺪﻘﻟا 

ﺔﺘﻜﺴﻟا تﻻﺎﺣ ﺺﻴﺨﺸﺗ ﻲﻓ ﺔﻴﻌﻄﻘﻤﻟا ﺔﻌﺷﻷا ﻦﻣ ﺔﻗد ﺮﺜآأ يﺪﻴﻠﻘﺘﻟا ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ﺮﺒﺘﻌﻳ 

ﺺﻴﺨﺸﺗ ﻰﻠﻋ ةرﺪﻘﻟا مﺪﻋ ﺎﻤﻬﺑﻮﻴﻋ ﻦﻣ ﻦﻜﻟ و ﺔﻳﻮﻣﺪﻟا 

رود ءﺎﺟ ﺎﻨه ﻦﻣ و ﺔﺑﺎﺻﻹا 

ﻦﻣ ﻰﻟوﻷا تﺎﻋﺎﺳ ﺖﺴﻟا ﻰﻟإ 

ةروﺪﻟا ﻲﻓ رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا ﺔﻴﻏﺎﻣﺪﻟا 

ثﻼﺜﻟا لﻼﺧ تﻻﺎﺤﻟا ﻦﻣ ﺮﻴﺜﻜﻟا 

ﺎﻬﺗرﺪﻘﻟ ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا 

تﻻﺎﺣ ﺺﻴﺨﺸﺗ ﻰﻓ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ماﺪﺨﺘﺳﺎﺑ ﺔﻳوﺮﺘﻟا و 

ﻲﻠﻋ ﺎﻬﺗرﺪﻗ ﻲﻟا ﻪﻓﺎﺿﻻﺎﺑ ﻪﺑﺎﺻﻹا 

ﻦﻣ ﻰﻟوﻷا 

تﺎﻋﺎﺳ ﺖﺴﻟا لﻼﺧ تﻻﺎﺤﻟا 

رﺎﺸﺘﻧﻻا 

ﻢﻈﻌﻣ ﺺﻴﺨﺸﺛ ﻰﻠﻋ 

. ﺔﻨﻣﺰﻤﻟاو 

ﻩدﺎﺤﻟا ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا تﻻﺎﺣ ﻦﻴﺑ ﺔﻗﺮﻔﺘﻟاو ﻪﻘﻴﻗﺪﻟا ثﺎﺑﺎﺻﻹا 

ﺺﻴﺨﺸﺗ 

ﻰﻓ ﻪﻣاﺪﺨﺘﺳا ﻦﻜﻤﻳ ﻚﻟﺬﺑو ﺦﻤﻟا ﺎﻳﻼﺧ لﻼﺧ ءﺎﻤﻟا تﺎﺌﻳﺰﺟ رﺎﺸﺘﻧا ﻪﻧﺄﺑ رﺎﺸﺘﻧﻻا ﻒﻳﺮﻌﺗ ﻦﻜﻤﻳ 

ﻲﻓ رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا تﻻﺎﺤﻟا 

ﻲﻓ 

رﺎﺸﺘﻧﻻا ﻞﻣﺎﻌﻣ ﻞﻘﻳ ﺚﻴﺣ ﺦﻤﻟا ﻲﻓ ﺔﺘﻴﻤﻟا ﻪﺠﺴﻧﻷا ﺪﻳﺪﺤﺗ 

ﻢﺛ ﻦﻣو ﺔﺑﺎﺼﻤﻟا ﺎﻳﻼﺨﻟا ﻞﺧاد ءﺎﻤﻟا تﺎﺌﻳﺰﺟ ﺔﺒﺴﻧ دادﺰﺗ ﺚﻴﺣ ﻰﻌﻴﺒﻄﻟا ﻪﻟﺪﻌﻣ ﻦﻋ 

ﺔﻘﻳﺮﻄﺑ 

ﺎﻬﻓﺎﺸﺘآا ﻦﻜﻤﻳ اﺪﺟ 

و ﺔﻐﺒﺻ يأ ﻦﻘﺣ جﺎﺘﺤﺗ 

ﻻ 

ةﺮﻜﺒﻤﻟا تاﺮﻴﻐﺘﻟا ﻩﺬه 

ﺎﻬﻧأ 


ﺔﻘﻳﺮﻄﻟا ﻩﺬه 

ﺔﻴﺴﻴﻃﺎﻨﻐﻣ صاﻮﺧ ﺎﻬﻟ ةدﺎﻣ ﻊﺒﺘﺘﺑ ﻪﺑﺎﺴﺣ ﻢﺘﻳو ﺦﻤﻟا ﺎﻳﻼﺧ ﻰﻟإ 

ﺔﻳﻮﻣﺪﻟا ةروﺪﻟا 

. ﺎﻳﻼﺨﻟا دوﺪﺣ ﻞﺧاد ﺎهرﺎﺸﺘﻧا ﺪﻳﺪﺤﺗ ﻢﺘﻳ 

زﺎﺘﻤﺗو 

ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ماﺪﺨﺘﺳﺎﺑ رﺎﺸﺘﻧﻻا 

. ﺮﻴﺼﻗ ﺖﻗو قﺮﻐﺘﺴﺗ 

مﺪﻟا لﻮﺻو ﺎﻬﺑ ﺪﺼﻘﻴﻓ ﺔﻳوﺮﺘﻟا ﺎﻣأ 

ﻲﻧﺎﻌﻳ فﻮﺳ ﺔﻳﻮﻣﺪﻟا ةروﺪﻟا ﻲﻓ رﻮﺼﻗ ﻦﻣ ﻲﻧﺎﻌﻳ يﺬﻟا ءﺰﺠﻟا . ﺦﻤﻠﻟ ﺎﻬﻟﻮﺻو ءﺎﻨﺛأ 

. ﻪﻴﻟإ 

ﺔﻐﺒﺼﻟا ﻞﺜﻣ 

ﺔﻐﺒﺼﻟا لﻮﺻو ﺮﺧﺄﺗ وأ مﺪﻋ ﻦﻣ

- 2 - 


ﻢﺋاد ﻒﻠﺘﺑ ﺐﻴﺻأ يﺬﻟا ﺦﻤﻟا ﻦﻣ ءﺰﺠﻟا ﺔﻓﺮﻌﻣ ﻦﻜﻤﻳ ﺔﻳوﺮﺘﻟا رﻮﺻ ﻊﻣ رﺎﺸﺘﻧﻻا رﻮﺻ ﺔﻧرﺎﻘﻣ ﺪﻨﻋ 

ﺔﻠﺑﺎﻗ ﺖﻟاز ﺎﻣو ﻰﻧﺎﻳﺮﺸﻟا داﺪﺴﻧﻹﺎﺑ 

تﺮﺛﺄﺗ ﻰﺘﻟا ﺔﺠﺴﻧﻷا ﺪﻳﺪﺤﺗ ﻦﻜﻤﻳ ﻚﻟﺬآو 

جﻼﻌﻠﻟ ﻞﺑﺎﻗ ﺮﻴﻏ و 

. جﻼﻌﻠﻟ 

ﺔﺘﻜﺴﻟا ﺐﺒﺳ ﺺﻴﺨﺸﺗ ﻲﻓ ﺔﻴﻤهأ وذ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ﺔﻄﺳاﻮﺑ ﺦﻤﻟا ﻦﻴﻳاﺮﺷ ﺮﻳﻮﺼﺗ ﺮﺒﺘﻌﻳ 

ﻲﻓ رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا تﻻﺎﺤﻟا ﻲﻓ ﻲﻧﺎﻳﺮﺸﻟا داﺪﺴﻧﻻا تﻻﺎﺣ ﻞﺜﻣ ﺔﻴﻠﺧﺪﺗ ﺮﻴﻏ ﺔﻘﺑﺮﻄﺑ ﺔﻴﻏﺎﻣﺪﻟا 

ﺔﺠﺴﻧأ ﻞﺧاد ﺔﻴﻀﻳﻷا داﻮﻤﻟا 

. ﻲﻧﺎﻳﺮﺸﻟا دﺪﻤﺘﻟا رﺎﺠﻔﻧا ﻦﻣ ﺞﺗﺎﻨﻟا ﻒﻳﺰﻨﻟا تﻻﺎﺣ و ﺔﻳﻮﻣﺪﻟا ةروﺪﻟا 

ﺔﻴﻤآ سﺎﻴﻗ ﻰﻠﻋ ﺪﻤﺘﻌﻴﻓ ﻲﻔﻴﻄﻟا ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟﺎﺑ ﺮﻳﻮﺼﺘﻟا 

ةروﺪﻟا ﻲﻓ رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا تﻻﺎﺤﻟ ﺮﻜﺒﻤﻟا ﺺﻴﺨﺸﺘﻟا 

ﻦﻣ ﻦﻜﻤﺘﻳ 

ﻚﻟﺬﺑ و ﺦﻤﻟا 

. ﻦﻴﺘﻋﻮﻤﺠﻣ 

ﻰﻟإ 

. ﺔﺑﺎﺼﻤﻟا ﺔﺠﺴﻧﻷا ﻲﻓ ﺔﻴﻀﻳﻷا داﻮﻤﻟا ﺔﻴﻤآ سﺎﻴﻗ 

ﻢﻬﻤﻴﺴﻘﺗ ﻢﺗ ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا 

ﻦﻣ نﻮﻧﺎﻌﻳ ﺎﻀﻳﺮﻣ نﻮﺴﻤﺧ 

ﻲﻓ رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا ﺔﻴﻏﺎﻣﺪﻟا 

ﺔﺘﻜﺴﻟا ﻦﻣ نﻮﻧﺎﻌﻳ ﺎﻀﻳﺮﻣ 

ﺔﺠﺗﺎﻨﻟا ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا ﻦﻣ نﻮﻧﺎﻌﻳ ﺎﻀﻳﺮﻣ 

11 

39 

ﺎﻣأ 

ﻖﻳﺮﻃ ﻦﻋ ﺔﻳﻮﻣﺪﻟا 

ﺔﻟﺎﺳﺮﻟا ﻩﺬه ﺖﻨﻤﻀﺗ 

ﻦﻣ نﻮﻜﺘﺗ ﻰﻟوﻷا ﺔﻋﻮﻤﺠﻤﻟا 

ﻦﻣ نﻮﻜﺘﺗ ﺔﻴﻧﺎﺜﻟا ﺔﻋﻮﻤﺠﻤﻟا ﺎﻣأ ﺔﻳﻮﻣﺪﻟا ةروﺪﻟا 

ﻦﻴﻧﺮﻟاو ﺔﻴﻌﻄﻘﻤﻟا ﺔﻌﺷﻷا ﺔﻴﺳﺎﺴﺣ ﺮﺜآأ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ماﺪﺨﺘﺳﺎﺑ رﺎﺸﺘﻧﻻا 

.( ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟا و ةدﺎﺤﻟا تﻻﺎﺤﻟا) 

تﻻﺎﺤﻠﻟ 

ﺮﻜﺒﻤﻟا ﺺﻴﺨﺸﺘﻟا 

ﻰﻌﻴﺒﻄﻟا ﻪﻟﺪﻌﻣ ﻦﻋ ﻪﻧﺎﺼﻘﻧ ﻢﺗ ﺚﻴﺣ ﺔﻄﻠﺠﻟا 

. ﺦﻤﻟﺎﺑ ﻒﻳﺰﻨﻟا ﻦﻋ 

نأ ﺎﻧﺪﺟو ﺪﻗو 

ﻲﻓ يﺪﻴﻠﻘﺘﻟا ﻰﺴﻴﻃﺎﻨﻐﻤﻟا 

ﻞﺣاﺮﻣ فﻼﺘﺧﺎﺑ رﺎﺸﺘﻧﻻا ﻞﻣﺎﻌﻣ ﺮﻴﻐﺗ ﺎﻨﻈﺣﻻ 

ﺪﻘﻟو 

. ﺔﻨﻣﺰﻤﻟا تﻻﺎﺤﻟا ﻲﻓ ﻪﺗدﺎﻳز ﻢﺗو ةﺮﺧﺄﺘﻤﻟا ةدﺎﺤﻟا و ةدﺎﺤﻟاو ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟا تﻻﺎﺤﻟا ﻲﻓ 

ماﺪﺨﺘﺳﺎﺑ ﺔﻳوﺮﺘﻟا ﺺﺤﻔﻟ 

7 

ﻲﻓ 

( ﺾﻳﺮﻣ 

: ﻲﺗﻻا ﺪﺟوو 

17) 

ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟا و ةدﺎﺤﻟا تﻻﺎﺤﻟا 

ﻢﻈﻌﻣ ﺖﻌﻀﺧ ﺪﻗو 

ﺔﻳوﺮﺘﻟا رﻮﺻ ﻊﻣ رﺎﺸﺘﻧﻻا رﻮﺻ ﺔﻧرﺎﻘﻣ ﻢﺗو ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا 

رﺎﺸﺘﻧﻻا رﻮﺻ ﻲﻓ ﺎﻬﻤﺠﺣ ﻦﻣ ﺮﺒآأ ﺔﻳوﺮﺘﻟا رﻮﺻ ﻲﻓ ﺔﺑﺎﺻﻹا 

ﻢﺠﺣ ﺖﻧﺎآ 

ﺔﺠﺴﻧأ دﻮﺟو اﺬه ﻲﻨﻌﻳو ةﺮﻴﺒﻜﻟا ﻦﻴﻳاﺮﺸﻟا داﺪﺴﻧا ﺔﺠﻴﺘﻧ 

6 

ﺔﺑﺎﺻﻹا 

ﻚﻠﺗ ﺖﻧﺎآو تﻻﺎﺣ 

. جﻼﻌﻠﻟ ﺔﻠﺑﺎﻗ ﺖﻟاز ﺎﻣو ﻰﻧﺎﻳﺮﺸﻟا داﺪﺴﻧﻹﺎﺑ 

تﺮﺛﺄﺗ 

ﻲﻓ رﺎﺸﺘﻧﻻا رﻮﺻ ﻲﻓ ﺎﻬﻤﺠﺤﻟ ﺔﻠﺛﺎﻤﻣ ﺔﻳوﺮﺘﻟا رﻮﺻ ﻲﻓ 



دﻮﺟو مﺪﻋ اﺬه ﻲﻨﻌﻳو ةﺮﻴﻐﺼﻟا 

ﻦﻴﻳاﺮﺸﻟا داﺪﺴﻧا ﺔﺠﻴﺘﻧ ﺔﺑﺎﺻﻻا ﻚﻠﺗ ﺖﻧﺎآو تﻻﺎﺣ 

ﻲﻓ رﺎﺸﺘﻧﻻا 

رﻮﺻ ﻲﻓ ﺎﻬﻤﺠﺣ ﻦﻣ ﺮﻐﺻأ ﺔﻳوﺮﺘﻟا رﻮﺻ ﻲﻓ 

. جﻼﻌﻠﻟ ﺔﻠﺑﺎﻗ ﺔﺠﺴﻧأ 



رﻮﺻ ﻲﻓ ةدﻮﺟﻮﻣ ﺎﻬﻨﻜﻟو ﺔﻳوﺮﺘﻟا رﻮﺻ ﻲﻓ ةدﻮﺟﻮﻣ ﺮﻴﻏ ﺔﺑﺎﺻﻻا ﺖﻧﺎآ و ﻦﻴﺘﻟﺎﺣ

ةﺮﻴﻐﺼﻟا 

ﻦﻴﻳاﺮﺸﻟا داﺪﺴﻧا ﺔﺠﻴﺘﻧ تﺎﺑﺎﺻﻹا 

ﻚﻠﺗ ﺖﻧﺎآ ةﺪﺣاو ﺔﻟﺎﺣ ﻲﻓ رﺎﺸﺘﻧﻻا 

ﻦﻴﻧﺮﻟا ﺔﻄﺳاﻮﺑ ﺦﻤﻟا ﻦﻴﻳاﺮﺷ ﺮﻳﻮﺼﺘﻟ ( ﺔﻟﺎﺣ 37) 

ﻲﻓ ةدﻮﺟﻮﻣ ﻲﻧﺎﻳﺮﺸﻟا داﺪﺴﻧﻻا تﻻﺎﺣ ﻢﻈﻌﻣ نأ ﺎﻧﺪﺟوو 

- 3 - 

. ﺔﻳوﺮﺘﻟا ةدﺎﻋإ 

ثوﺪﺣو 


ﻰﻟوﻷا ﺔﻋﻮﻤﺠﻤﻟا تﻻﺎﺣ ﻢﻈﻌﻣ ﺖﻌﻀﺧ ﺪﻗو 

ﻦﻴﻳاﺮﺸﻟا داﺪﺴﻧا نﺎﻴﺒﻟ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا 

ﺮﺜآأ ةﺮﻴﺒﻜﻟا ﻦﻴﻳاﺮﺸﻟا تﻻﺎﺣ ﻲﻓو ﺔﻨﻣﺰﻤﻟا تﻻﺎﺤﻟا ﻲﻓ ﺎﻬﻨﻣ ﺮﺜآأ ةدﺎﺤﻟاو ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟا تﻻﺎﺤﻟا 

و ﻲﻔﻴﻄﻟا ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟﺎﺑ ﺮﻳﻮﺼﺘﻟا ( ﺔﻟﺎﺣ 34) 

و ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟاو ةدﺎﺤﻟا تﻻﺎﺤﻟا ﻞآ 

ﻲﻓ ﺔﺑﺎﺻﻻا نﺎﻜﻣ ﻲﻓ 

. ةﺮﻴﻐﺼﻟا 

ﻦﻴﻳاﺮﺸﻟا تﻻﺎﺣ ﻲﻓ ﺎﻬﻨﻣ 

ﻰﻟوﻷا ﺔﻋﻮﻤﺠﻤﻟا تﻻﺎﺣ ﻢﻈﻌﻣ ﺖﻌﻀﺧ و 

ﻚﻴﺘآﻼﻟا ﺾﻤﺣ دﻮﺟو 

. ﻪﻴﻠﻋ يﻮﺘﺤﺗ ﻻ ﻰﺘﻟا ﺦﻤﻟا ﻦﻣ ﺔﻤﻴﻠﺴﻟا ءاﺰﺟﻷﺎﺑ ﺔﻧرﺎﻘﻣ ﺔﻨﻣﺰﻤﻟاو 

ةﺮﺧﺄﺘﻤﻟا 

ﺎﻨﻈﺣﻻ ﺪﻗ 

ةدﺎﺤﻟا تﻻﺎﺤﻟا ﻢﻈﻌﻣ 

ﻦﻴﺗﺎﻳﺮﻜﻟا ﺺﻘﻧ ﺎﻀﻳأ ﺎﻨﻈﺣﻻ و تﻻﺎﺤﻟا 

ﻞآ ﻲﻓ ﻪﻧﺎﺼﻘﻧ ﺎﻨﻈﺣﻻ ﺪﻘﻓ ﻚﻴﺗﺮﺒﺳﻷا ﺾﻤﺤﻟ ﺔﺒﺴﻨﻟﺎﺑ ﺎﻣأ 

ءاﺰﺟﻷﺎﺑ ﺔﻧرﺎﻘﻣ 


نﺎﻜﻣ ﻲﻓ تﻻﺎﺤﻟا ﻦﻴﺑ ﻦﻴﻟﻮﻜﻟا ﺔﻴﻤآ ﻲﻓ فﻼﺘﺧﻻاو تﻻﺎﺤﻟا ﻢﻈﻌﻣ ﻲﻓ 

. ﺔﻤﻴﻠﺴﻟا 

ﺎﻀﻳﺮﻣ 11 ﻦﻣ نﻮﻜﺘﺗو ﺦﻤﻟﺎﺑ ﻒﻳﺰﻨﻟا ﻦﻋ ﺔﺠﺗﺎﻨﻟا ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا : ﺔﻴﻧﺎﺜﻟا ﺔﻋﻮﻤﺠﻤﻠﻟ ﺔﺒﺴﻨﻟﺎﺑ ﺎﻣأ 

. تﺎﻋﻮﻤﺠﻣ 

ةﺪﻋ ﻰﻟإ 

ﻒﻳﺰﻨﻟا نﺎﻜﻣ ﺐﺴﺣ ﻢﻬﻤﻴﺴﻘﺗ ﻢﺗ 

ﻒﻳﺰﻨﻠﻟ داﺪﺘﻣا ﻪﺑ ﺪﺣاو ﺾﻳﺮﻣ ﻢﻬﻨﻣ ﺎﻀﻳﺮﻣ 8ﻰﻠﻋ 

يﻮﺘﺤﺗو ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺣ 

. ﺦﻤﻟا ﻦﻴﻄﺑ ﻞﺧاد 

. ﺔﻴﺗﻮﺒﻜﻨﻌﻟا مﻷا ﺖﺤﺗ ﻒﻳﺰﻨﻟا ﻦﻣ نﻮﻧﺎﻌﻳ ﻦﻴﺘﻟﺎﺣ 

. ﺦﻤﻟا ﻦﻴﻄﺑ ﻞﺧاد ﻒﻳﺰﻨﻟا ﻦﻣ ﻲﻧﺎﻌﺗ ةﺪﺣاو ﺔﻟﺎﺣ 

ضﺮﻤﻟا ﺖﻴﻗﻮﺗ ﺐﺴﺣ ( ﻞﺣاﺮﻣ) 

عاﻮﻧأ ةﺪﻋ ﻰﻟإ 

ﻢﻬﻤﻴﺴﻘﺗ ﻢﺗ ﺪﻘﻓ ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺤﻟ 

يﻮﺘﺤﺗو ( ﻒﻳﺰﻨﻟا ثوﺪﺣ ﺬﻨﻣ ﻰﻟوﻷا 24 لﻼﺧ) 

ﻰﻠﻋ يﻮﺘﺤﺗو 

( ﻒﻳﺰﻨﻟا 

ثوﺪﺣ ﺬﻨﻣ 

مﺎﻳأ 

3-2 

يﻮﺘﺤﺗو ( ﻒﻳﺰﻨﻟا 

ثوﺪﺣ ﺬﻨﻣ مﻮﻳ 14-3 

ﻦﻣ) 

ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟا ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺣ 

ﻦﻣ) 

. ﻦﻴﻀﻳﺮﻣ 

ﻰﻠﻋ 

ةدﺎﺤﻟا ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺣ 

. ﻦﻴﻀﻳﺮﻣ 

ةﺮﺧﺄﺘﻤﻟا ةدﺎﺤﻟا ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺣ 

. 

ﻰﺿﺮﻣ 

3 ﻰﻠﻋ 

 

 

 

ﺔﺒﺴﻨﻟﺎﺑ 

: ﻞﻤﺸﺗو

ﻰﻠﻋ يﻮﺘﺤﺗو 

( ﻒﻳﺰﻨﻟا 

ثوﺪﺣ ﺬﻨﻣ ﻦﻴﻋﻮﺒﺳا ﻦﻣ ﺮﺜآأ) 

- 4 - 

ﺔﻨﻣﺰﻤﻟا ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا 

. ﺪﺣاو ﺾﻳﺮﻣ 


ﺐﻴآﺮﺗو ﻒﻳﺰﻨﻟا ﺔﻠﺣﺮﻣ فﻼﺘﺧﺎﺑ يﺪﻴﻠﻘﺘﻟا ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا رﻮﺻ ﻲﻓ ﻒﻳﺰﻨﻟا ﺮﻬﻈﻣ ﻒﻠﺘﺨﻳو 

ةﺮﻜﺒﻤﻟا ةدﺎﺤﻟا 

تﻻﺎﺤﻟا 

ةدﺎﺤﻟا تﻻﺎﺤﻟا ﺾﻌﺑو 

ﻲﻓ ﻞﻘﻳ 

ﺔﻨﻣﺰﻤﻟا تﻻﺎﺤﻟا 

ﻪﻧأ ﺎﻧﺪﺟو ﺚﻴﺣ رﺎﺸﺘﻧﻻا ﻞﻣﺎﻌﻣ ﺎﻀﻳأ ﻒﻠﺘﺨﻳو 

ﻲﻓ 

ﺪﻳﺰﻳو 

ﺎﻧﺪﺟوو ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ﺔﻄﺳاﻮﺑ ﺦﻤﻟا ﻦﻴﻳاﺮﺷ ﺮﻳﻮﺼﺘﻟ 

 

ﻦﻴﺑﻮﻠﺟﻮﻤﻴﻬﻟا 

ةﺮﺧﺄﺘﻤﻟا ةدﺎﺤﻟا تﻻﺎﺤﻟا ﺾﻌﺑو ةدﺎﺤﻟاو 

ﻒﻳﺰﻨﻟا 

. ةﺮﺧﺄﺘﻤﻟا 

تﻻﺎﺣ ﻞآ ﺖﻌﻀﺧ ﺪﻗو 

ﻦﻴﺘﻟﺎﺣ ﻲﻓ ﻦﻴﻳاﺮﺸﻟا 

ﻲﻓ ﻖﻴﺿو ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺣ ﻦﻣ ةﺪﺣاو ﺔﻟﺎﺣ ﻲﻓ ﻦﻴﻳاﺮﺸﻟا ﻲﻓ داﺪﺴﻧا 

دﺪﻤﺗو 

ﺔﻴﺗﻮﺒﻜﻨﻌﻟا مﻷا ﺖﺤﺗ 

ﻒﻳﺰﻨﻟا تﻻﺎﺣ ﻦﻣ ةﺪﺣاو ﺔﻟﺎﺣ و 

. ﺔﻴﺗﻮﺒﻜﻨﻌﻟا مﻷا ﺖﺤﺗ 

ﺦﻤﻟا ﻞﺧاد ﻒﻳﺰﻨﻟا تﻻﺎﺣ ﻦﻣ 

ﻒﻳﺰﻨﻟا تﻻﺎﺣ ﻦﻣ ةﺪﺣاو ﺔﻟﺎﺣ ﻲﻓ ﻲﻧﺎﻳﺮﺷ 

: ﻲﺗﻻا ﺎﻨﺼﻠﺨﺘﺳا 

لﻼﺧ 

ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا تﻻﺎﺣ ﺺﻴﺨﺸﺗ ﻲﻓ ﺮﻴﺒآ رود ﻪﻟ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ماﺪﺨﺘﺳﺎﺑ رﺎﺸﺘﻧﻻا نإ 

ﺔﻗﺮﻔﺘﻟاو ﻪﻘﻴﻗﺪﻟا ثﺎﺑﺎﺻﻹا 

ﺺﻴﺨﺸﺗ ﻲﻠﻋ ﻪﺗرﺪﻗ ﻲﻟا ﻪﻓﺎﺿﻻﺎﺑ ﻪﺑﺎﺻﻹا 

ﻦﻣ ﻰﻟوﻷا تﺎﻋﺎﺳ ﺖﺴﻟا 

ﻦﻣ ﺎﻨﻜﻤﺘﻓ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ماﺪﺨﺘﺳﺎﺑ ﺔﻳوﺮﺘﻟا ﺎﻣأ ﺔﻨﻣﺰﻤﻟاو ﻩدﺎﺤﻟا ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا تﻻﺎﺣ ﻦﻴﺑ 

ﻦﻴﻳاﺮﺷ ﺮﻳﻮﺼﺗ 

مﺪﺨﺘﺴﻳو جﻼﻌﻠﻟ ﺔﻠﺑﺎﻗ ﺖﻟاز ﺎﻣو ﻰﻧﺎﻳﺮﺸﻟا داﺪﺴﻧﻹﺎﺑ 

تﺮﺛﺄﺗ ﻰﺘﻟا ﺔﺠﺴﻧﻷا ﺔﻓﺮﻌﻣ 

ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟﺎﺑ ﺮﻳﻮﺼﺘﻟا ﺎﻣأ 

ﺪﻗو 

ﻦﻴﻳاﺮﺸﻟا داﺪﺴﻧا نﺎﻴﺑ ﻲﻓ ﻰﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ﺔﻄﺳاﻮﺑ ﺦﻤﻟا 

ﻲﻓ رﻮﺼﻗ ﻦﻋ ﺔﺠﺗﺎﻨﻟا ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا تﻻﺎﺣ ﻲﻓ ﺔﻴﻀﻳﻻا داﻮﻤﻟا ﻲﻓ تﺎﻓﻼﺘﺧﻻا ﺮﻬﻈﻴﻓ ﻲﻔﻴﻄﻟا 

. ﺔﻳﻮﻣﺪﻟا ةروﺪﻟا 

ﺔﻠﺣﺮﻣ فﻼﺘﺧﺎﺑ رﺎﺸﺘﻧﻻا ﻞﻣﺎﻌﻣو 

يﺪﻴﻠﻘﺘﻟا ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا رﻮﺻ ﻲﻓ ﻒﻳﺰﻨﻟا ﺮﻬﻈﻣ ﻒﻠﺘﺨﻳو 

. 

ﻦﻴﺑﻮﻠﺟﻮﻤﻴﻬﻟا ﺐﻴآﺮﺗو ﻒﻳﺰﻨﻟا

- 5 - 

ﻲﺑﺮﻌﻟا ﺺﺨﻠﻤﻟا

ﻲﺴﻴﻃﺎﻨﻐﻤﻟا ﻦﻴﻧﺮﻟا ﻦﻣ ﺔﻔﻠﺘﺨﻣ 

ﻖﻳزﺎﻗﺰﻟا ﺔﻌﻣﺎﺟ 

ﺐﻄﻟا ﺔﻴﻠآ 

ﺔﻴﺼﻴﺨﺸﺘﻟا ﺔﻌﺷﻷا ﻢﺴﻗ 

تﺎﻴﻨﻘﺘﺑ 

ﺔﻴﻏﺎﻣﺪﻟا ﺔﺘﻜﺴﻟا ﺮﻳﻮﺼﺗ 

ﻦﻣ ﺔﻣﺪﻘﻣ ﺔﻟﺎﺳر 

ﺔﺒﻴﺒﻄﻟا 

يﺮﻳﺮﺤﻟا ﺪﻤﺤﻣ ﺪﻤﺤﻣ رﺎﻔﻐﻟا ﺪﺒﻋ ﻰﻨﻣ 

ﺔﻴﺼﻴﺨﺸﺘﻟا ﺔﻌﺷﻷا ﺪﻋﺎﺴﻣ سرﺪﻣ 

ﻖﻳزﺎﻗﺰﻟا ﺔﻌﻣﺎﺟ-ﺐﻄﻟا 

ﺔﻴﻠآ 

ﺔﻴﺼﻴﺨﺸﺘﻟا ﺔﻌﺷﻷا ﻲﻓ ﻩارﻮﺘآﺪﻟا ﺔﺟرد ﻰﻠﻋ لﻮﺼﺤﻠﻟ ﺔﺌﻃﻮﺗ 

يوﺎﻄﻨــﻃ 

فاﺮﺷإ ﺖﺤﺗ 

ﺪــﻤــﺣأ 

ﻲــﺤــﺘـــﻓ 

ﺔﻴﺼﻴﺨﺸﺘﻟا ﺔﻌﺷﻷا ذﺎﺘﺳأ 



ﺔـﻔـﻴـﻠـﺧ 

ﻞـــﻴــﺒــﻧ 

ﺎـــﻴــــﻟاد 

ﺔﻴﺼﻴﺨﺸﺘﻟا ﺔﻌﺷﻷا ذﺎﺘﺳأ 



سوراﺪﻴﻋ ﺪﻴﻤﺤﻟاﺪﺒﻋ يﺪﺠﻣ 

بﺎﺼﻋﻷا و ﺦﻤﻟا ضاﺮﻣأ ﺪﻋﺎﺴﻣ ذﺎﺘﺳأ 



ﻖﻳزﺎﻗﺰﻟا ﺔﻌﻣﺎﺟ – ﺐﻄﻟا ﺔﻴﻠآ 

2009 

/ 

/ 

/ 

د 

د. 

أ 

. أ 

د. 

أ

Prof.Dr. Fathy Ahmed Tantawy

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