Stroke and Cerebrovascular Diseases

(For Internal Use Only)

Sui-yi Xu, MD, Ph.D, Associate Professor

Department of Neurology, The First Hospital of SXMU

 C O N T E N T S

01 Introduction
02 Risk Factors for Stroke
03 The Major Causes of Ischemic Stroke
04 Transient Ischemic Attacks (TIA)
05 Pathophysiology of Ischemic Infarction
06 Imaging techniques in stroke
07 The syndromes of ischemic stroke
01 Introduction
PART
01 Introduction

Among all the neurologic diseases of adult life, stroke ranks first in frequency and importance. The common
mode of expression of stroke is a relatively sudden occurrence of a focal neurologic deficit. Strokes are
broadly categorized as ischemic or hemorrhagic. Ischemic stroke is due to occlusion of a cerebral blood vessel
and causes cerebral infarction.

Ischemic strokes are classified by the underlying cause of the vascular occlusion. One of three main processes
is usually operative: (i) atherosclerosis with superimposed thrombosis affecting large cerebral or extra cerebral
blood vessels, (ii) cerebral embolism, and (iii) occlusion of small cerebral vessels within the parenchyma of
the brain.

Closely allied with ischemic strokes is the transient ischemic attack (TIA), a temporary neurologic deficit
caused by a cerebrovascular disease that leaves no clinical or imaging trace.
 01 Introduction

The second broad category consists of hemorrhage, which occurs either within the substance of the brain, called
intracerebral hemorrhage (ICH); or blood contained within the subarachnoid spaces, called subarachnoid
hemorrhage (SAH).

The causes of the first category are numerous and include chronic hypertension, coagulopathies that arise
endogenously or because of anticoagulant medications, vascular malformations of the brain, cranial trauma,
and hemorrhage that occurs within the area of an ischemic stroke.

Subarachnoid hemorrhage has fewer fundamental causes, the most common being the rupture of a developmental
aneurysm arising from the vessels of the circle of Willis, but also includes cerebral trauma and arteriovenous
malformations, and rarer processes.
02 Risk Factors for Stroke
PART
02 Risk Factors for Stroke

This is an area of major public health importance in that several modifiable factors are known to increase the
liability to stroke. The most important of these are hypertension, atrial fibrillation, diabetes mellitus, cigarette
smoking, and hyperlipidemia.

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03 The Major Causes of
PART Ischemic Stroke
 03 The Major Causes of Ischemic Stroke

Cerebral Embolism

This is the most common cause of ischemic strokes and of all the types of
stroke, cerebral embolism develops most rapidly, “like a bolt out of the blue.”

In most cases, the embolic material consists of a fragment that has broken
away from a thrombus within the heart or independently from the
endocardial surface of a cardiac chamber or valve (“cardioembolic”).

Somewhat less frequently, the source is intraarterial from the distal end of a
thrombus within the lumen of an occluded or severely stenotic carotid or
vertebral artery (“artery to artery embolus”), or a clot that originates in the
systemic venous system and passes through an aperture in the heart walls,
for example, patent foramen ovale (PFO).

Atheromatous plaques in the ascending aorta have been recognized to be a

more frequent source of embolism than had been previously appreciated.
03 The Major Causes of Ischemic Stroke

Atherothrombosis

Atherosclerosis is the usual underlying pathology for local vascular

thrombosis.

Atherothrombosis may cause cerebral infarction in several ways.

The most obvious is that an occlusive plaque or a thrombus formed
on a plaque occupies the lumen of a major intracerebral vessel,
such as the middle cerebral artery, and stops flow to the areas of the
brain supplied by the vessel.

Or, an atherothrombotic lesion in a proximal vessel may serve as

the nidus for the formation of an embolus that manifests itself as a
stroke in one of the territories of that vessel—called “artery-to-
artery” embolism.
04 Transient Ischemic Attacks
PART
04 Transient Ischemic Attacks (TIAs)

Transient ischemic attacks are focal neurologic episodes that correspond to a vascular territory, appear abruptly
and cease in matter of minutes. Previously, the definition on clinical grounds extended to spells that lasted up
to 24 h, then a shorter time frame was adopted but now, an event that leaves no clinical or imaging trace of
infarction is considered a TIA.

Transient Blindness

In the transient ischemic attack of the eye, transient monocular blindness (also
called amaurosis fugax or TMB) is the usual symptom (ischemic attack from ICA).

TIAs consisting of a homonymous hemianopia should suggest a stenosis of the

posterior cerebral artery but it is often difficult for the patient to make the
distinction from monocular blindness.
04 Transient Ischemic Attacks (TIAs)

Mechanism of Transient Ischemic Attacks

The likely causes of TIA are reduced blood flow or embolic particles. It has become clear that many instances
of single transient attacks have an embolic mechanism. In contrast, repetitive TIAs, repeatedly producing the
same or similar clinical syndrome are in most cases related to vascular stenosis with reduced blood flow to a
limited region of the brain.

Differential Diagnosis of TIA

TIA must be distinguished from other brief neurologic attacks that are from seizures, migraine, and its variants,
transient global amnesia, syncope, vertigo from labyrinthine disease, and psychogenic episodes, as emphasized
further on.
05 Pathophysiology of Ischemic Infarction
PART
05 Pathophysiology of Ischemic Infarction

Cerebral infarction basically comprises two pathophysiologic processes: one, a loss of the supply of oxygen
and glucose secondary to vascular occlusion, and the other, an array of changes in cellular metabolism
consequent to the collapse of energy-producing processes, ultimately with disintegration of cell structures and
their membranes, a process subsumed under the term necrosis.

At the center of an ischemic stroke is a zone of infarction. The necrotic tissue swells rapidly, mainly because of
excessive intracellular water content (cytotoxic edema). Because anoxia also causes necrosis and swelling of
cerebral tissue, oxygen lack must be a factor common to both infarction and anoxic encephalopathy. The effects
of ischemia, whether functional and reversible or structural and irreversible, depend on its degree and duration.

Implicit in discussions of ischemic stroke and its treatment is the existence of a “penumbra” zone that is
marginally perfused and contains at-risk but viable neurons. Presumably this zone exists at the margins of an
infarction, which at its core has irrevocably damaged tissue that is destined to become necrotic.
 05 Pathophysiology of Ischemic Infarction

Vascular Factors

The neurons in the penumbra are considered to be physiologically

“stunned” by moderate ischemia and subject to salvage if blood
flow is restored in a certain period of time.

Arrangement of the major arteries on the right side carrying blood from the heart to the brain. Also shown are collateral vessels that may
modify the effects of cerebral ischemia. For example, the posterior communicating artery connects the internal carotid and the posterior
cerebral arteries and may provide anastomosis between the carotid and basilar systems.
05 Pathophysiology of Ischemic Infarction

Diagram of the base of the brain showing the circle of Willis and its main branches
06 IMAGING TECHNIQUES IN STROKE
PART
06 IMAGING TECHNIQUES IN STROKE

Diffusion-weighted magnetic resonance techniques are particularly useful to detect infarction within minutes
of the stroke, that is, considerably earlier than CT and other MRI sequences.

MRI showing acute infarctions. The upper

images show a right middle cerebral artery
infarction that appears bright on diffusion
weighted imaging (DWI) (upper left). There is
subtle hyperintensity representing early
vasogenic edema on T2-FLAIR sequence
(upper right). The lower images show an acute
cerebellar infarction in the territory of the
posterior inferior cerebellar artery (PICA) that
is bright on DWI (lower left) and faintly bright
on T2-FLAIR (arrow, lower right).
07 THE SYNDROMES OF ISCHEMIC STROKE
PART
07 THE SYNDROMES OF ISCHEMIC STROKE

Middle Cerebral Artery Stroke Syndromes

The middle cerebral artery (MCA) has superficial and deep hemispheral branches that together supply the
largest portion of the cerebral hemisphere. The idealized picture of total occlusion of the stem is one of
contralateral hemiplegia (involving the face, arm, and leg as a result of infarction of the posterior limb of the
internal capsule), hemianesthesia, and can include homonymous visual field deficit (because of infarction of
the lateral geniculate body), with deviation of the head and eyes toward the side of the lesion.

Diagram of the left cerebral hemisphere,

lateral aspect, showing the courses of the
middle cerebral artery and its branches
and the principal regions of cerebral
localization. Below is a list of the clinical
manifestations of infarction in the territory
of this artery and the corresponding
regions of cerebral damage.
 07 THE SYNDROMES OF ISCHEMIC STROKE

Diagram of one cerebral hemisphere, coronal section, showing the regions of blood supply of the major cerebral vessels.
07 THE SYNDROMES OF ISCHEMIC STROKE

Corrosion preparations with plastics demonstrating penetrating branches of the anterior and middle cerebral
arteries.
 07 THE SYNDROMES OF ISCHEMIC STROKE
Posterior Cerebral Artery Stroke Syndromes

Occlusion of branches to the temporal and occipital lobes gives rise to a homonymous hemianopia as a result
of involvement of the primary visual receptive areas.

A. Inferior aspect of the left hemisphere showing the branches and distribution of the posterior cerebral artery and
the principal anatomic structures supplied.
B. B. Axial diffusion-weighted MRI showing an acute ischemic infarction in the posterior cerebral artery territory.
 07 THE SYNDROMES OF ISCHEMIC STROKE

The posterior cerebral and basilar arteries.

A. The terminus of the basilar artery and branches originating from the P1 through P3 segments.
B. Lateral view of the brain showing the branches of the posterior cerebral artery.
C. Axial diffusion-weighted MRI showing an acute ischemic infarction due to occlusion of an artery of
Percheron, an anatomic variant, in which an azygos paramedian artery supplies both sides of the
posterior-medial thalamus.
07 THE SYNDROMES OF ISCHEMIC STROKE
07 THE SYNDROMES OF ISCHEMIC STROKE
Bilateral Posterior Cerebral Artery Stroke Syndromes

These occur as a result of successive infarctions or from a single embolic or thrombotic occlusion of the upper
basilar artery, especially if the posterior communicating arteries are unusually small or absent, or from global
failure of circulation.

Bilateral lesions of the occipital lobes, if extensive, cause “cortical blindness” that is essentially bilateral
homonymous hemianopia. The pupillary reflexes are preserved and the optic discs appear normal.

Sometimes the patient is unaware of being blind and denies the problem even when it is pointed out to him
(Anton syndrome). More frequently, the lesions are incomplete, and a sector of the vision, usually on one side,
remains intact.
07 THE SYNDROMES OF ISCHEMIC STROKE
Vertebral Artery Stroke Syndromes

The vertebral artery is assigned four numerical segments for

convenience of explication. They are:

V1, from the origin to the first entry into the cervical
transverse foramen (usually C6 as noted);
V2, from the transverse foramen to the uppermost foramen
(at C1);
V3 from this site to the dural penetration at the foramen
magnum;
V4 from the dural entry to the junction with the opposite
vertebral artery and the origin of the basilar artery.
07 THE SYNDROMES OF ISCHEMIC STROKE
Vertebral Artery Stroke Syndromes

If the occlusion of the artery is so situated as to block the posterior inferior cerebellar
artery supplying the lateral medulla and inferior cerebellum (PICA), a characteristic
syndrome results with vertigo being a prominent symptom.

If the subclavian artery is blocked proximal to the origin of the left vertebral artery,
exercise of the arm on that side may draw blood from the right vertebral and basilar
arteries, retrograde down the left vertebral and into the distal left subclavian artery—
sometimes resulting in the symptoms of basilar insufficiency.

Lateral Medullary Syndrome

Known also as the Wallenberg syndrome (who described a case in 1895), this common
stroke is produced by infarction of a wedge of lateral medulla lying posterior to the
inferior olivary nucleus.
 07 THE SYNDROMES OF ISCHEMIC STROKE

Transverse section through the upper medulla, reflecting regions supplied by the vertebral arteries and their branches
 07 THE SYNDROMES OF ISCHEMIC STROKE

The complete syndrome, as outlined by Fisher and colleagues (1961) comprises

(a) symptoms derived from the vestibular nuclei (vertigo, nystagmus, oscillopsia, vomiting);
(b) spinothalamic tract (contralateral or, less often, ipsilateral impairment of pain and thermal sense over half the
body);
(c) descending sympathetic tract (ipsilateral Horner syndrome—miosis, ptosis, decreased sweating);
(d) issuing fibers of the ninth and tenth nerves (hoarseness, dysphagia, hiccough, ipsilateral paralysis of the
palate and vocal cord, diminished gag reflex);
(e) Utricular nucleus (vertical diplopia and illusion of tilting of vision and rotation of the vertical meridian, rarely
so severe as to produce upside down vision);
(f) olivocerebellar, spinocerebellar fibers, restiform body and inferior cerebellum (ipsilateral ataxia of limbs,
falling or toppling to the ipsilateral side, and the sensation of lateropulsion);
(g) descending tract and nucleus of the fifth nerve (pain, burning, and impaired sensation over ipsilateral half of
the face);
(h) nucleus and tractus solitarius (loss of taste); and rarely,
(i) cuneate and gracile nuclei (numbness of ipsilateral limbs).
07 THE SYNDROMES OF ISCHEMIC STROKE
Basilar Artery Stroke Syndromes

The result of occlusion of the midbasilar artery, gives rise to the locked-in syndrome, in which the
patient is mute and quadriplegic but conscious, reflecting interruption of descending motor pathways
in the base of the pons but sparing of the reticular activating system.

Horizontal eye movements are obliterated but vertical ones and some ability to elevate the eyelids
are spared. In the presence of the full syndrome of basilar occlusion with coma, quadriplegia, and
ophthalmoplegia, it is usually not difficult to make the correct diagnosis
07 THE SYNDROMES OF ISCHEMIC STROKE
Lacunar Stroke

Lacunes are usually caused by occlusion of small arteries, 50 to 200 μm in diameter.

Fisher, in several papers, delineated the most frequent symptomatic forms of lacunar stroke:
1. Pure motor hemiplegia
2. Pure sensory stroke
3. Clumsy hand–dysarthria
4. Ipsilateral hemiparesis–ataxia
Take home message

Very important!
 The most important of risk factors for stroke
 The composition of willis circle
 The concept of TIA
 The meaning of the penumbra zone
 The clinical manifestation of middle cerebral artery stroke syndrome
 The most frequent symptomatic forms of lacunar stroke
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