Public Institution Nicolae Testemitanu State University of Medicine and Pharmacy of the Republic of Moldova [301605]

Ministery of Health of the Republic of Moldova

Public Institution “Nicolae Testemitanu” State University of Medicine and Pharmacy of the Republic of Moldova

Faculty of Medicine

Department of Radiology and Medical Imaging

Diploma thesis

Acute Ischemic Stroke

Name and surname of student: [anonimizat], group: 6, 1050

Scientifical coordinator: [anonimizat] 2016

STATEMENT

I hereby declare that the license thesis titled:” Acute ischemic stroke “

Is written by me and has never been submitted to another university or institution of higher education in the country or abroad. Also, [anonimizat], are given in the paper with the rules for avoiding plagiarism:

– [anonimizat] a detailed reference source;

– Reformulation of the texts in own words written by other authors have detailed reference;

– summarizing the ideas of other authors have detailed reference to the original text.

Date : Safia Alaa :

CONTENTS

PREFACE……………………………………………………………………….………………………..

1- Actuality and the research level of the investigated theme….4

2- The aim and the objectives of the thesis …..…………………………4

3- The scientific news of the obtained results……………..……………4-5

CHAPTER I – BIBLIOGRAPHIC ANALYSIS……………………………..….…

1.1 Acute ischemic stroke …………………………………………………………6

1.2 Epidemiology …………………….………………………………………………..6

1.3 Clinical features of Acute ischemic stroke ……………………………6

1.4 Pathology………………………….…………………………………………………7

1.5 Morphology…………………………………………………………………………8-9

1.6 Pathogenesis………………………………………………………………..……..10-12

1.7 Diagnostic Methods……………………………………………..……………..12-20

1.8 treatment and prognosis ……………………………………………….….20-21

[anonimizat]……………….…22-25

[anonimizat] …………………………………26-35

[anonimizat]……………………………………………….………36

BIBLIOGRAPHY……………………………………………………………………………37-38

[anonimizat] (MRI) [anonimizat].

Acute Ischemic stroke results from an abrupt cessation of adequate amounts of blood reaching parts of the brain. Acute ischemic strokes can be divided according to territory affected or mechanism.

2- The aims and objectives of the thesis

The intentions and the aim of this work is to carry out the importance of the magnetic resonance imaging and CT in the assessment of Acute ischemic stroke ; [anonimizat].

[anonimizat], is the most important to detect early changes observed in patient with acute ischemic stroke

To see which are the most commonly involved vessels and sites that harbor early changes in acute ischemic stroke and how outcome is dependent on it

3- The scientific news of the obtained results

Recent studies have demonstrated about the usefulness of MRI in detecting early changes during the hyper-acute phase of acute ischemic stroke (during the first 6 hours) and in selecting patients for treatment. New MRI models for selecting patients have emerged that focus not only on the ischemic penumbra but also on the infarct core. Fixed time-window selection parameters are being replaced by timing-based individualized MRI stroke features. New ways to interpret traditional MRI stroke sequences are emerging.

CHAPTER I – BIBLIOGRAPGIC ANALYSIS

1.1 Acute ischemic stroke

Acute ischemic stroke results from a sudden stop of adequate amounts of blood supply to some parts of the brain.

Ischemic strokes can be divided according to mechanism of the stroke or territory affected .

1.2 Epidemiology

Stroke is the second most common cause of morbidity worldwide (after myocardial infarction) and is the leading cause of acquired disability.

The incidence of AIS is approximately 700,000 per year, with about 61,000 deaths.

1.3 Clinical features of acute ischemic stroke

An acute ischemic stroke typically presents with rapid onset of neurological deficit, which is determined by the area of brain that is involved. The symptoms often evolve over hours, and may worsen or improve, depending on the fate of the ischemic penumbra. Stroke should be considered in any patient presenting with acute neurologic deficit or any alteration in level of consciousness. The vascular territory affected will determine exact symptoms and clinical behavior of the lesion:

anterior circulation infarct : anterior cerebral artery infarct , middle cerebral artery infarct , posterior cerebral artery infarct , lacunar infarct

posterior circulation infarct : posterior cerebral artery infarct , cerebellar infarct , brainstem infarct , midbrain infarct , pontine infarct , medullary infarct

posterior cerebral artery infarct

Common signs and symptoms of stroke include the sudden onset of any of the following symptoms:

Hemiparesis, monoparesis, or quadriparesis

Hemisensory deficits

Monocular or binocular visual loss

Visual field deficits

Diplopia

Dysarthria

Facial droop

Ataxia

Vertigo (rarely in isolation)

Aphasia

Sudden decrease the level of consciousness

1.4 Pathology

Deprivation of oxygen and glucose in the brain as a result of interruption of blood flow through an intracranial artery , initiates a cascade of events at a cellular level which, if circulation is not reestablished in time, will lead to cell death, through necrosis.

The mechanism of vessel obstruction is important in addressing therapeutic maneuver’s to both attempt to reverse or minimize the effects and to prevent future infarcts.

Risk factors for AIS include:

1 – modifiable conditions : Hypertension , Diabetes mellitus , hypercholesterolemia , carotid stenosis , excessive alcohol intake , tobacco use , physical inactivity , obesity .

2- no modifiable conditions : Age , race , sex , history of migraine headache , ethnicity , fibro muscular dysplasia , hereditary ( family history of stroke or transient ischemic attack )

Causes of AIS include: embolism , cardiac embolism , atrial fibrillation , ventricular aneurysm , paradoxical embolism , endocarditis , atherosclerotic embolism , fat embolism , air embolism , thrombosis , perforator thrombosis: lacunar infarct , acute plaque rupture with overlying thrombosis , arterial dissection , Global cerebral hypoxia

1.5 Morphology

Cerebral parenchyma alterations in acute ischemic stroke involve changes at different levels :

Neuronal injury during AIS

During the early phase of infarction will appear the eosinophilic neurons , which result from neuronal mitochondrial metabolism dysfunction . the eosinophilic neurons can persist in the ischemic area from 2 till 6 months. The earliest neuronal injury consisted in increasing cytoplasm eosinophilia , with the nucleus appearing shrunken and darkly basophilic , or developing clumped chromatin condensations.

Later , the nucleus will show advanced degeneration and will appear homogenous and the cytoplasm will appear more less in uniform structure.

Finally, the neurons are disintegrated resulting eosinophilic debris. Then , all the eosiophilic debris will be phagocytized by the macrophages .

Another changes which we can see on the Neurons are :

Vacuolation of cytoplasm

Schrinkage and loss their affinity for hematoxylin

Fragmentation and degenerative changes of myelin tracts in white matter

Microglial response to acute ischemic stroke

At the beginning the microglia will changed their shape to rod-shaped and they will be distribiuted along the capillaries , Around dying neurons the microglial cells retract their processes and assume an amoeboid morphology, becoming activated. Sometimes we can see signs of phagocytosis of the dying neurons. At the end of the first day after the onset of acute ischemic stroke , the microglial reaction is well developed

Astrocyte response to acute ischemic stroke

The early observed changes in response to cerebral hypoxia is astrocyte swelling with watery cytoplasm, at the beginning just around the capillaries and then will be around the necrotic neurons. At the site of infarction itself , the astrocyte will have necrotic aspect , while in the penumbra they will become reactive . after 2 weeks of the onset of infarction they will become gemistocytic astrocyte , having a large cytoplasim mass and a long branching processes and a large nuclei . at the end of the necrosis process the whole parenchyma will be liquefied , resulting in eosinophilic cellular debris .

Vascular changes in acute ischemic stroke

The earliest vascular changes in the infracted area consisted in swelling of the capillaries endothelium and invagination of the endothelial nuclei into the vessel lumen. And we can observed irregularities in the capillary lumen, hyalination and sclerosis of arterioles within the white matter.

We can see wall thickening, disintegration, cellular infiltration, and perivascular edema, due to plasma component extravasation in the area of the cerebral acute ischemic stroke . these edema will be more pronounced in the white matter . as a result of plasma leakage into the adjacent brain , will be development of spongiosis.

Inflammatory reaction in acute ischemic stroke

The first inflammatory reaction is leucocyte migration in the brain capillaries from the infarct area , and in the meninges at 4-7 hours after onset of ischemia .then after the 7 day it will be development of polymorphonuclear leukocyte infiltrate , from the third day until 2 months we can observe the presence of a mononuclear inflammatory infiltrate .between the first and the second week the macrophages will have the maximal response , and the asthey became engorged with a foamy material .

1.6 Pathogenesis

The main mechanisms causing ischemic strokes are:

The more frequently mechanisms: (1) thrombosis, (2) embolism and (3) global ischemia (hypotensive) stroke

The less frequently mechanisms : (1) strokes caused by vasospasm (migraine, following SAH, hypertensive encephalopathy) (2)some form of “arteritis”

Thrombosis pathological changes which will lead to thrombosis formation :

Atherosclerosis is the most common leadings cause of vascular obstruction resulting in thrombotic stroke. Atherosclerotic plaques can undergo pathological changes like ulcerations, thrombosis, calcifications, and intra-plaque hemorrhage. The susceptibility of the plaque to disrupt, fracture or disrupt or ulcerate depends on the structure of the plaque, and its composition and consistency. Disruption of endothelium that can occur in the setting of any of these pathological changes initiates a complicated process that activates many destructive vasoactive enzymes. Platelet adherence and aggregation to the vascular wall follow, forming small hatchery of platelets and fibrin. Leucocytes that are present at the site within 1 hour of the ictus mediate an inflammatory response.

clot formation due to hypercoagulable state or due to fibro muscular dysplasia or due to arteritis (Giant cell and Takayasu), and dissection of a vessel wall.

In contrast to the occlusion of large atherosclerotic vessels, lacunar infarcts occur as a result of occlusion of deep penetrating arteries that are 100 to 400 mm in diameter and originate for the cerebral arteries. The putamen and pallidum, followed by pons, thalamus, caudate nucleus, and internal capsule are the most frequently affected sites. The size of a lacunar infarct is only about 20 mm in diameter. The incidence of lacunar infarcts is 10% to 30% of all strokes depending on race and preexisting hypertension and diabetes mellitus. The small arteriole, most frequently as a result of chronic hypertension lengthens, becomes tortuous and develops subintimal dissections and micro-aneurysms rendering the arteriole susceptible to occlusion from micro-thrombi. Fibrin deposition resulting in lipohyalinosis is considered to be the underlying pathological mechanism.

Embolic stroke (ES) occur as a result of embolization of an artery in the central circulation from a variety of sources include :

Clot, fibrin, and pieces of atherosclerotic plaque

Other materials known that can move into the central circulation and cause embolism include fat, air, tumor or metastasis, bacterial clumps, and foreign bodies.

Superficial branches of cerebral and cerebellar arteries are the most frequent targets of emboli. Most emboli lodge in the middle cerebral artery distribution because 80% of the blood carried by the large neck arteries flow through the middle cerebral arteries.

The two most common sources of emboli are:

the left sided cardiac chambers

large arteries, (e.g. “artery to artery” emboli that result from detachment of a thrombus from the internal carotid artery at the site of an ulcerated plaque).

The neurological outcome from an ES depends not only on the occluded vascular territory but also on the ability of the embolus to cause vasospasm by acting as a vascular irritant. The vasospasm can occur in the vascular segment where the embolus lodges or can involve the entire arterial tree. Vasospasm tends to occur in younger patients, probably because the vessels are more pliable and less atherosclerotic. Many embolic strokes become “hemorrhagic” causing hemorrhagic infarction (HI). Hemorrhagic infarct is an ischemic infarct in which bleeding develops within the necrotizing cerebral tissue. The pathogenesis of hemorrhagic transformation of a pale infarct is a complex phenomenon.

Global – Ischemic or Hypotensive stroke caused as a result of profound decrease in systemic blood pressure due to any reason is responsible for “hypotensive stroke.” Some neurons are more susceptible to ischemia than others. These include the pyramidal cell layer of the hippocampus and the Purkinje cell layer of the cerebellar cortex. Cerebral gray matter is also particularly vulnerable. Abundance of glutamate in these neurons renders them more susceptible to global ischemia. Global ischemia causes the greatest damage to areas between the territories of the major cerebral and cerebellar arteries known as the “boundary zone” or “watershed area.” The parietal-temporal-occipital triangle at the junction of the anterior, middle, and posterior cerebral arteries is most commonly affected. Watershed infarction in this area causes a clinical syndrome consisting of paralysis and sensory loss predominantly involving the arm; the face is not affected and speech is spared. Watershed infarcts make up approximately 10% of all ischemic strokes and almost 40% of these occur in patients with carotid stenosis or occlusion.

1.7 Diagnostic methods (Radiographic features )

The title : Is CT or MRI the Method of Choice for Imaging Patients With Acute Ischemic Stroke?

Authors : Turgut Tatlisumak, MD, PhD , Ashok Srinivasan, MD, Mayank Goyal, MD, Faisal Al Azri, Cheemun Lum

1- Non-contrast CT brain

Non-contrast CT of the brain remains the method of choice of imaging in the setting on an acute stroke. Detection of changes depends on: the territory, the experience of the interpreting radiologist and of course the time of the scan from onset of symptoms. Whether tissue is supplied by end arteries (e.g. lenticulostriate arteries) or has collateral supply (much of the cerebral cortex) will influence how quickly cytotoxic edema develops. For example detection of MCA territory infarct has been shown to be approximately 60-70% in the first 6 hours, although changes in the deep grey matter nuclei (especially lentiform nucleus) can be visible within 1 hour of occlusion in up to 60% of patients 6.

The goals of CT in the acute setting are:

To exclude intracranial hemorrhage, which would preclude thrombolysis;

Look for any "early" features of infarction

To exclude other intracranial pathologies that may mimic a stroke

2-CT perfusion ( contrast-CT )

CT perfusion is one of the most important tool in selecting patients for reperfusion therapy as well as increasing the accurate diagnosis of ischemic stroke among non-expert readers four fold compared to the routine used non-contrast CT .

It allows :

The core of the infarct (that part destined to never recover regardless of reperfusion) to be identified

The core of the surrounding penumbra (the region which although ischemic has yet to go on to infarct and can be potentially reversible).

The key to interpretation is understanding a number of perfusion parameters:

cerebral blood volume (CBV)

cerebral blood flow (CBF)

mean transit time (MTT)

time to peak (TPP)

Areas which demonstrate matched defects in CBV and MTT represent the unsalvageable infarct core, but the areas which have prolonged MTT but preserved CBV are considered to be the ischemic penumbra .

C-CT angiography

Advantages :

may identify thrombus within an intracranial vessel, and may guide intra-arterial thrombolysis or clot retrieval.

evaluation of the carotid and vertebral arteries in the neck

establishing stroke etiology (eg. atherosclerosis, dissection)

access limitation for endovascular treatment (e.g. tortuosity, stenosis)

Images for CT

Axial unenhanced CT images, obtained in a 45-year-old man 2 hours after the onset of left hemiparesis, show obscuration of the right lentiform nucleus (arrow in b). This feature is less visible with the routine brain imaging window used for a than with the narrower window used for b

Unenhanced CT image in a 72-year-old woman with acute right hemiplegia shows hyper attenuation in a proximal segment of the left MCA (arrows). (b) and coronal . The presence of an intravascular thrombus in this location was confirmed by comparing the reformatted images with the CT source images

CT perfusion maps of cerebral blood volume (a) and cerebral blood flow (b) show, in the left hemisphere, a region of decreased blood volume (white oval) that corresponds to the ischemic core and a larger region of decreased blood flow (black oval in b) that includes the ischemic core and a peripheral region of salvageable tissue. The difference between the two maps (black oval _ white oval) is the penumbra.

D-MRI

MRI is more time consuming and less available than CT, but has significantly higher sensitivity and specificity in the diagnosis of acute ischemic infarction in the first few hours after onset.

Images for MRI

1.8 Treatment and prognosis

The treatment and prognosis of acute ischemic stroke are mainly codetermined by underlying and associated systemic diseases that are almost always present and by the time of presentation ( after the AIS attack ) . It is proven that management of general medical problems is the basis for stroke treatment.

General management of stroke patients include : respiratory and cardiac care, fluid and metabolic management, blood pressure control, and treatment of elevated intracranial pressure, and treatment of seizures and prophylactic measures concerning deep venous thrombosis, pulmonary embolism, aspiration pneumonia, other infections, and decubitus ulcer are part of the general treatment of the patients

Specific management of stroke patients include : ( to allow maximal survive period of the patient )

Neurosurgical by performing decompressed craniectomies (with or without duroplasty).

New reperfusion therapies include : thrombolysis therapy ( like streptokinase or rtPA ) and mechanical thrombectomy

Factors that influence stroke prognosis including : age, stroke severity, stroke mechanism, infarct location, comorbid conditions, clinical findings, and related complications.

Chapter II – Material and research methods

This chapter will include the discussion of 3 different articles that was performed by groups of doctors and researchers to study:

The First article

The Titel :

MRI Screening Before Standard Tissue Plasminogen Activator Therapy Is Feasible and Safe

Authors :

Dong-Wha Kang, MD, PhD; Julio A. Chalela, MD; William Dunn, MD; Steven Warach, MD, PhD; NIH-Suburban Stroke Center Investigators

Patient and Methods—

These study was performed at the National Institutes of Health Stroke Center at suburban Hospital in Bethesda , where 120 patients was selected to participate in these study , the Authors in these study compared the results of all these patient treated with intravenous tissue plasminogen activator (tPA) within 3 hours after onset of symptoms of acute ischemic stroke at their center .

Only for 97 patient in these study where performed MRI , because the rest 23 patients they have some criteria for contraindication for MRI or because the patient late arrived after two hours and a half so it was not enough time to

complete the MRI before 3 hours from onset of AIS .

MRI specific inclusion criteria was used if the diagnosis for acute ischemic stroke was not fully clear like in patient with hypoglycemia , seizure at rest or limited neurological evaluation because of using some drugs ( like sedative).

All the patient had treated with tissue plasminogen activator independence of the age or the limit of National Institutes of Health Stroke Scale . the patient where excluded from treatment with thrombolytic just in case they on the the following specific MRI exclusion criteria :

Acute lesion appearing hyperintense on T2 weighted image

Presence of acute or subacute lesions on DWI

The presence of new disabling deficits despite normal DWI

MRI evidence of acute or chronic cerebral hemorrhage

The second article

Titel : Comparison of CT and CT Angiography Source Images With Diffusion-Weighted Imaging in Patients With Acute Stroke Within 6 Hours After Onset

Author : Peter Schramm, MD; Peter D. Schellinger, MD; Jochen B. Fiebach, MD; Sabine Heiland, PhD; Olav Jansen, MD; Michael Knauth, MD; Werner Hacke, MD; Klaus Sartor, MD

Patients and methods :

In these study , the author have investigated the clinical and imaging findings ( CT and MRI ) of 20 patients ( 13 men and 7 women ) . which have symptoms of acute ischemic stroke within the first 6 hours , with time interval between CT and MRI 1 hour . the researcher’s analyzed infarct volume on the first day and on the fifth day and then they assessed the clinical outcome

All the patient which the researcher’s used in these study were with :

No any significant preexisting neurological deficit

Stable vital signs

No contraindication for MRI

No a history of allergy or renal failure .

Each patient underwent a complete physical and clinical examination , before to begin in the study , include :

Each patient received a non–contrast-enhanced CT scan ,to exclude intra-cerebral hemorrhage .

history, neurological sings , stabilization of vital parameters

The third article

The titel :

Clinical MRI of Acute Ischemic Stroke

MR Perfusion Imaging in Acute Ischemic Stroke

Authors :

R. Gilberto González, MD, PhD , Neuroradiology Division, Massachusetts General Hospital, Boston, Martinos Center for Biomedical Imaging, Charlestown, MA , Harvard Medical School, Boston, MA ,

William A. Copen, MD , Pamela W. Schaefer, MD, Ona Wu, PhD

Patients and methods :

The main goal of radiological imagining ( MRI ) for patient with acute ischemic stroke is to as fast as possible to select those patients who are most likely to benefit from immediate treatment to improve the outcome and to decrease the mortality rate by these patient . this group include patients with :

Major artery occlusion , who need immediate intravenous thrombolytic management

Minor artery occlusion , which cannot be resolved spontaneously

Classification of AIS by mortality by artery :

Classification of Acute ischemic stroke depends on the size of the occluded artery and the outcome :

25-35% of AIS are major , characterized by NIHA stroke scale of 10 or more , and are due to occlusion of major cerebral artery ( include distal internal carotid artery ICA, proximal middle cerebral artery MCA , basilar artery BA ) that produce a large infarction , outcome without treatment is poor . because of these such patient must be identified as quickly as possible to convert them from major stroke patient into minor stroke patient .

Minor stroke have mild symptoms with NIHA stroke scale less than 10 , caused by occlusion of small distal branch artery , this result in small infarction , and good outcome with or without treatment

The reperfusion methods and the reperfusion time :

Chapter III –Results and discussion

The results of first article

120 patients (There were 62 men and 58 women, and mean age was 74.2_15.3 years ) treated with intravenous tPA within 3 hours of acute ischemic stroke symptom onset were included in this study. After the NIHSS the neurologic deficit was as the following :

43 patient was mild ( score less than 6 )

37 patient was moderate ( score between 7 and 15 )

40 patient was severe ( score 16 )

Median baseline NIHSS score was 10.5 (range 0 to 33).

Stroke type was :

Atherosclerosis in 13 patients (10.8%)

Cardio-embolism in 65 (54.2%),

Small-vessel occlusion in 11 (9.2%),

other etiology in 6,

Idiopathic etiology in 25 (20.8%).

Functional outcome was as the following :

Outcome with obtained at 3 months in 86 (72%)

Outcome was obtained before 3 months in 29 (24%)

Outcome was obtained at 1 or 2 months In 5 (4%) patients

The screening time with computed tomography CT was shorter( was performed in 23 patients befor tPA administration and in 58 of patient screened with MRI ) , than in MRI screening ( was performed in 97 before tPA administration ) . but the outcome of the patients were approximately the same just with a little difference between them .

With MRI screening (mRS 0 to 1, 42.3%; mRS 0 to 2, 49.5%)

With CT screening (mRS 0 to 1, 34.8%; mRS 0 to 2, 39.1% )

Conclusion— according to the results of these study , the researchers demonstrate that MRI screening before tPA therapy is suitable and not associated with unacceptable times to treatment or outcomes

This patient presented with stuporous mental status without definite focal neurological deficits. DWI revealed hyperintensities (left), and apparent diffusion coefficient map showed low signal intensities (right) in bilateral thalami, suggesting hyperacute ischemic stroke. This patient was treated with intravenous tPA

This patient presented with sudden nonfluent aphasia and right hemiparesis 2 hours previously. DWI (left column) showed hyperintensities in left frontal lobe, but T2-weighted imaging (middle column) showed somewhat more extensive hyperintensities in the same area, suggesting vasogenic edema of subacute lesion. This patient was not treated with tPA and was found to have brain tumor demonstrated by follow-up contrast-enhanced T1-weighted imaging (right column).

This patient had multiple microbleeds on gradient echo T2*- weighted imaging. This patient was not treated with tPA.

The result of the second article

The researchers analyzed the information of 20 stroke patients who underwent CT and MRI scanning within 6 hours of onset of acute ischemic stroke symptoms

The time interval between CT and MRI ranged from 15 min to 1 hour .

Vessel occlusion seen on both CTA and MRA was present in 16 of 20 patients

CT volumes did not differ from MRI volumes , and the CT lesion volume too much correlated with the initial MRI volume as well as the outcome lesion volume

Patients with poor collaterals experienced infarct growth and had a significantly bad clinical outcome , compared to patients with good collaterals they had a better outcome

The 20 patients were divided into 2 groups 🙁 for further statistical analysis )

Group a ( poor ) consist of 13 patient that has poor vessel enhancement around the lesion site , these patients had a very high NIHSS score 15

Group b ( good ) consist of 7 patient that has good collateral status around the lesion site , these patient had a medium NIHSS score 12

Conclusion :

MRI is the best modality of choice for early detection of acute ischemic stroke changes

The concomitant use of the following radiological modalities :

non–contrast-enhanced CT (to exclusion of intracranial hemorrhage)

CTA (to check vessel status)

contrast-enhanced CTA-SI (demarcation of irreversible infarct)

allow diagnostic assessment of acute stroke with a high quality comparable to stroke assessment with MRI. and it allow to distinguish patients which are at risk of infarct growth from those who are not according to the collateral status .

CT and MR images of a 61-year-old patient (patient 2). The initial CT only shows signs of reduced gray-white matter differentiation in the left MCA territory (top left), but the exact extent of hypoperfused brain tissue cannot be estimated in this non–contrast enhanced CT scan. The CTA-SI (window, 75; level, 40) shows the hypoperfused brain area (top right) in its exact frontiers. Almost no intravascular enhancement of the pial vessels in the vicinity of the lesion is seen; this is classified as poor collaterals. The reconstructed CTA demonstrates left proximal MCA occlusion (middle left). In contrast to the right hemisphere, almost the entire left MCA territory is hyperintense on initial DWI (middle right). The final infarct outcome in the follow-up CT scan on day 5 correlated with the CTA-SI lesion (bottom left)

This 46-year-old patient (patient 7) had an initial CT 4 hours after symptom onset (top left). Signs of infarction can be seen in the initial CT: loss of density of the insular cortex and parts of the opercula back to the temporal region. Beyond it, the CTA-SI shows a slightly contrasted area in the middle MCA territory on the left side (top right) and poor contrast-enhanced collateral vessels. On the initial DWI scan (5 hours after symptom onset; bottom left), the left insular cortex and putamen are hyperintense. Final infarct outcome in T2-weighted image included approximately one third of the left MCA territory (bottom right) with persistent perfusion deficit, according to CTA-SI.

The result of third article

MRI perfusion imaged can be used in acute ischemic stroke to provide information about regional brain perfusion and to select patient for thrombolytic therapy

Patients who have major artery occlusions need treatment, Because the typical outcome for most of these patients is poor

Patient who have minor artery occlusion can be spontaneous resolution without any treatment

Conclusion: high mortality rate in basilar artery

Low mortality rate in internal carotid artery

Patient outcomes with acute ischemic stroke depend on :

Early detection of the acute ischemic stroke

Severity of the symptoms, as measured by the NIH stroke scale

Site of occlusion,

Size of the core of the infarct at the time of presentation,

The success of the treatment

Diffusion MRI performed on a 22 year old woman who had a right internal carotid artery occlusion caused by traumatic dissection of that artery. The patient had inadequate collateral circulation and a hemodynamically isolated right hemisphere. DWI performed at 30 minutes after witnessed onset of paralysis demonstrated lesions that may have been reversible. Attempts at treatment failed. Repeat DWI at 90 and 150 minutes demonstrated expansion and severe reduction in the diffusion coefficient of water throughout the right cerebral hemisphere. The rate of neuronal loss in this individual is nearly 50 times higher than the Saver estimate.

Imaging data are from a patient with a right MCA occlusion and paralysis on the left side. DWI (top row) and mean transit time (MTT, bottom row) maps obtained 4.2 hours after symptom onset. The sizes of the diffusion and MTT abnormalities are very similar 4 hours after the initial imaging study. Adapted from Gonzalez et al. (23)

Frequency of stroke types and goal of treatment

Between 25-35% of acute ischemic strokes are major, characterized by NIH stroke scale of 10 or greater and are due to occlusion of a major cerebral artery that produces a large infarction. Outcomes without treatment are usually poor with modified Rankin scale of 3 or greater. Minor strokes have mild symptoms of less than 10 and are is caused by an occlusion of a distal, small branch artery. This typically results in small infarcts and good outcomes (modified Rankin scale of 0 to 2) with or without treatment. Lacunar infarcts have similar outcomes to minor strokes. The major goal of current treatments is to convert major strokes into minor strokes (curved arrow).

All patients who present with a new onset of a significant neurological deficit receive a non contrast CT (NCCT) scan that is followed immediately by CT angiography (CTA). If no hemorrhage is identified, head and neck CTA is performed. While the patient is undergoing CT examination, it is determined whether the patient is able to undergo an MRI including that there are no contraindications. If the patient is able and the scanner is available, a diffusion MRI scan (DWI) is acquired. The next step is dependent on the findings on vessel imaging and DWI. If there is an occlusion of a major artery (ICA, proximal MCA or basilar artery), and there is a small diffusion abnormality (defined as less than 70ml in an anterior circulation stroke), then the patient proceeds to endovascular therapy if the patient meets all other criteria for such treatment. If endovascular therapy is not indicated, if the DWI abnormality is large or there is no large artery occlusion, then the patient will proceed to MRI perfusion. CT perfusion (CTP) is provided to patients who are not able to undergo MRI. Perfusion imaging information obtained by CT or MRI may help to more fully delineate the patient’s physiology that may be useful in the consideration of other therapies. Patients that are eligible and are within the 3 or 4.5 hour time limit for IV fPA will receive the treatment in the CT scanner suite before proceeding to MRI, if that is the next step.

Chapter IV – conclusion

It is important to detect stroke in short time, and to select patient who need immediate thrombolytic therapy because the outcome of patient with acute ischemic stroke , mostly depend on early initiation of management with thrombolytic therapy

MRI is best radiological modality to detect changes during the hyper-acute phase of acute ischemic stroke after the sudden onset of neurological defect during the first 6 hours of the attack .

Outcome depends on type of affected artery, Outcome depends on the site of occlusion

Bibliography

Clinical MRI of Acute Ischemic Stroke , R. Gilberto González, MD, PhD , Neuroradiology Division, Massachusetts General Hospital, Boston, MA , Martinos Center for Biomedical Imaging, Charlestown, MA , Harvard Medical School, Boston, MA

MR Perfusion Imaging in Acute Ischemic Stroke , William A. Copen, MD, Director of Advanced MR Neuroimaging, Massachusetts General Hospital Department of Radiology, Division of Neuroradiology, Instructor in Radiology, Harvard Medical School Pamela W. Schaefer, MD, and Associate Director of Neuroradiology, Neuroradiology Fellowship Director, Clinical Director of MRI, Massachusetts General Hospital, Associate Professor of Radiology, Harvard Medical School, Boston, MA, Ona Wu, PhD Assistant in Neuroimaging, Assistant Professor of Radiology, MGH/MIT/HMS Athinoula A.

Is CT or MRI the Method of Choice for Imaging Patients With Acute Stroke? Turgut Tatlisumak, MD, PhD , Ashok Srinivasan, MD, Mayank Goyal, MD, Faisal Al Azri, Cheemun Lum

MRI Screening Before Standard Tissue Plasminogen Activator Therapy Is Feasible and Safe – Dong-Wha Kang, MD, PhD; Julio A. Chalela, MD; William Dunn, MD; Steven Warach, MD, PhD; NIH-Suburban Stroke Center Investigators

Comparison of CT and CT Angiography Source Images With Diffusion-Weighted Imaging in Patients With Acute Stroke Within 6 Hours After Onset – Peter Schramm, MD; Peter D. Schellinger, MD; Jochen B. Fiebach, MD; Sabine Heiland, PhD; Olav Jansen, MD; Michael Knauth, MD; Werner Hacke, MD; Klaus Sartor, MD

State-of-the-Art Imaging of Acute Stroke- Ashok Srinivasan, MD , Mayank Goyal, MD , Faisal Al Azri, MD Cheemun Lum, MD

Acute Ischemic Stroke – H. Bart van der Worp, M.D., Ph.D., and Jan van Gijn, F.R.C.P.

MRI-guided selection of patients for treatment of acute ischemic stroke- Richard Leigha and John W. Krakauer